Cancer stem cells (CSCs) play crucial roles in tumor metastasis, therapy resistance, and immune evasion. Identifying and understanding the factors that regulate the stemness of tumor cells presents promising opportunities for developing effective therapeutic strategies. In this study on oral squamous cell carcinoma (OSCC), we confirmed the key role of KLF7 in maintaining the stemness of OSCC. Using chromatin immunoprecipitation sequencing and dual-luciferase assays, we identified ITGA2, a membrane receptor, as a key downstream gene regulated by KLF7 in the maintenance of stemness. Tumor sphere formation assays, flow cytometry analyses, and in vivo limiting dilution tumorigenicity evaluations demonstrated that knocking down ITGA2 significantly impaired stemness. Upon binding to its extracellular matrix (ECM) ligand, type I collagen, ITGA2 activates stemness-associated signaling pathways, including PI3K-AKT, MAPK, and Hippo. TC-I 15, a small-molecule inhibitor of the ITGA2-collagen interaction, significantly sensitizes oral squamous cell carcinoma (OSCC) to cisplatin in xenograft models. In summary, we reveal that the KLF7/ITGA2 axis is a crucial modulator of stemness in OSCC. Our findings suggest that ITGA2 is a promising therapeutic target, offering a novel anti-CSC strategy.

Metabolic reprogramming is a hallmark of cancer and de novo lipogenesis (DNL) accelerates the progression of ovarian cancer. In this study, we investigated the effects of cardamonin, a natural compound potential to suppress various malignancies, on the lipid anabolism in ovarian cancer. Cell proliferation was assessed using CCK-8 and clone formation assay. Cell apoptosis was detected by flow cytometry with Annexin V-FITC/PI staining and mitochondrial membrane potential (MMP) was measured with JC-10 probe. Free fatty acids (FFA) was measured by fluorescence using acyl-CoA oxidation and carnitine palmitoyl transferase-1 (CPT-1) activity was analyzed by spectrophotometric assay using palmitoyl-CoA and DTNB (5,5'-dithio-bis-(2-nitrobenzoic acid)) reaction. mRNA expression was measured by Quantitative Real-Time PCR. Protein expression was analyzed through western blotting and immunofluorescence. Raptor was knocked down by shRNA and Raptor was overexpressed by lentiviral transfection. The antitumor effect of cardamonin was evaluated using a xenotransplantation tumor bearing mouse model. Cardamonin suppressed the cell proliferation, induced cell apoptosis and triggered mitochondrial damage in ovarian cancer cells. Cardamonin inhibited the protein expression of sterol regulatory element binding protein 1 (SREBP1) and its downstream lipogenic enzymes and decreased FFA content and CPT-1 activity. Additionally, cardamonin inhibited the activation of mechanistic target of rapamycin complex 1 (mTORC1) and expression of regulatory-associated protein of mTOR (Raptor). Raptor knockdown abolished the inhibitory effect of cardamonin on mTORC1 and SREBP1. Furthermore, cardamonin inhibited mTORC1 activation and lipogenic proteins expression induced by Raptor overexpression. Cardamonin reduced the tumor growth and fatty acid synthase of the tumors, as evidenced by decreased expression of Ki-67 and FASN. It suggests that cardamonin suppresses mTORC1/SREBP1 through reducing the protein level of Raptor and inhibits DNL of ovarian cancer.

Colorectal cancer (CRC) is one of the most common types of cancer worldwide. Alternative therapy has been widely used in CRC treatment, with deuterium-depleted water (DDW) demonstrating promising anticancer effects in a number of cancer types. The aim of the present study was to assess the anticancer effects of DDW in CRC cells and the possible mechanism involved. HT-29 and DLD-1 cells were cultured in conditioned medium prepared with DDW. Cell malignant behaviors were assessed using EdU, colony formation, tumor-sphere formation, wound-healing and Transwell assays. Stemness-related proteins, Nanog and octamer-binding transcription factor-4, were assessed using western blotting. Intracellular reactive oxygen species (ROS) levels were determined using 2',7'-dichlorodihydrofluorescein diacetate fluorescent probes. Reverse transcription-quantitative PCR and western blotting were used to assess the expression of forkhead box protein M1 (FoxM1), cyclin D1 (CCND1) and matrix metalloproteinase 9 (MMP9). The results indicated that treatment with DDW significantly inhibited the proliferation, tumor-sphere formation, migration and invasion of HT-29 and DLD-1 cells, as well as the expression of stemness-related proteins. In the mechanistic analysis, DDW treatment was revealed to decrease ROS production and downregulate the expression of FoxM1. As the downstream targets of FoxM1, the expression levels of CCND1 and MMP9 were also shown to be decreased. Moreover, H2O2-induced oxidative stress rescued FoxM1 expression in the presence of DDW treatment, and overexpression of FoxM1 was demonstrated to abolish the DDW-mediated tumor suppressive effects. The findings from the present study indicate that the anticancer effects of DDW in CRC cells occur by inactivating the ROS/FoxM1 signaling pathway. Moreover, the results provide a possible agent for CRC treatment.

Antiproliferative effects of glucosamine, a glucose derivative with a similar structure to glucose, have been discovered, but the molecular mechanisms are not yet fully understood. Since glucosamine and glucose not only have similar structures but also are catalyzed by the same enzyme, hexokinase (HK), the present study delved into determining whether the antiproliferative effect of glucosamine involved the inhibition of glycolysis by competition with glucose. Whole‑genome screening analysis showed that a number of the gene pathways controlled by glucosamine were directly and indirectly involved in glycolysis. In vitro experiments revealed that as more glucose was added, the antiproliferative effect of glucosamine decreased. Also, it was found that glucosamine was transported into cells mainly through glucose transporter (GLUT) 2 which was responsible for the antiproliferative effects of glucosamine. In addition, the present study found that cancer cell lines with low expression level of HKII show high sensitivity to glucosamine and a HK inhibitor, 3‑bromopyruvate, enhanced the antiproliferative effect of glucosamine. Under hypoxic conditions, activated hypoxia‑inducible factor 1α (HIF‑1α) inducing glucose uptake and glycolysis hampered glucosamine‑induced cell death and HIF1A knockdown or HK inhibitors restored the antiproliferative effects of glucosamine. These findings demonstrated that glucosamine is an efficient glycolysis inhibitor and that GLUT2 and HKII play important roles as biomarkers for determining sensitivity to glucosamine. Moreover, the results suggested that the antiproliferative effect of glucosamine may be more efficient when administered in combination with other glycolytic agents or inhibitors targeting HIF‑1α.

In this study, fluridone was utilized to induce Aurantiochytrium limacinum OUC86 to identify the key genes involved in the synthesis of Long-chain Polyunsaturated Fatty Acids (LC-PUFAs). With the increase of fluridone concentration, the lipid content increased, the proportion of EPA was the highest under the treatment of 75 mg/L fluridone ethanol solution. Transcriptome sequencing analysis of A. limacinum was conducted, and differential expression genes related to fatty acid metabolism were identified. The transcript levels of Δ4 desaturase gene (Δ4-DES) and long-chain acyl-coenzyme A synthetase gene (LACS) showed significant changes, with KEGG metabolic pathway analysis indicating their crucial roles in the conversion of LC-PUFAs, potentially closely related to the increase in EPA and DHA content. Therefore, these two genes were recombinant expressed in Saccharomyces cerevisiae to study their functions. Compared to the untransformed yeast strain YS-Δura3, the recombinant strains YS-Δ4 and YS-LACS exhibited an increase in the proportion of LC-PUFAs. The lipid content in YS-Δ4 increased by 18.82%, while DPA content decreased by 67.02%, and DHA content increased by 115.85% at 48 h. In YS-LACS, EPA content increased by 132.86%, DPA content rose by 62.65%, and DHA content increased by 33.33% at 24 h. These results suggest that the expression of Δ4-DES can promote the synthesis of long-chain fatty acids and significantly facilitate the conversion of DPA to DHA; and the expression of LACS significantly promotes the synthesis of EPA, DPA, and DHA, which provide potential genetic targets for regulating the fatty acid composition of A. limacinum through genetic engineering.

Effects of waterlogging (WL) stress and its mitigation by nitrate (NO3-) were investigated in a commercial cucumber hybrid line. WL resulted in a shift toward anaerobic metabolism in roots and development of adventitious roots (ARs). In WL stressed roots exodermal, extracellular H2O2 accumulation and protein nitration were detected. Shoot growth was retarded with signs of oxidative stress. Nitrate content decreased in both root and shoot. In the root WL upregulated several genes implicated in hypoxic response, including transcripts of CsRAP2.3, CsRBOHs and the CsHem3 phytoglobin genes. Nitrate supplementation restored shoot growth and mitigated oxidative stress. Fermentative metabolism was reduced in the roots. Nitrate levels increased substantially, expression of NRT1 genes was induced, supporting improved NO3- uptake and delivery. According to chemical analysis and fluorescent microscopy NO accumulated in the vascular cylinder of roots. NO depletion by cPTIO confirmed a role for NO in stress mitigation. cPTIO treatment decreased AR formation and foliar nitrate levels. It decreased protein nitration and strongly downregulated nitrate transporters' gene expression in roots. Overall, our work revealed nitrate triggered, NO mediated alleviation of WL stress in cucumber. Resolution of WL induced energy crisis in the roots by nitrate treatment was attributed to parallel effects of anaerobic respiration and AR formation. Shoot growth repression was probably alleviated by improved root functions, including elevated nitrate transport. Expression of NRT1 nitrate transporter genes was induced by nitrate, and this induction was found NO dependent in WL stressed cucumber.

Targeted therapy leveraging synthetic lethality in homologous recombination (HR)-defective tumors, particularly in BRCA-mutated tumors through poly(ADP-ribose) polymerase (PARP)-dependent repair inhibition, has shown success. However, the challenge lies in the ability of the tumors to reactivate HR via diverse mechanisms, leading to resistance against PARP-dependent repair inhibition. Addressing this issue, the down-regulation of HR activity has been explored as a potential strategy to overcome PARP inhibitor-resistant tumors. Yet, the intricate modulation of HR gene expression in mammalian cells is still not fully understood. In this study, we used a small molecule, UNI66, identified from high-throughput screening, to investigate regulatory mechanisms of HR. UNI66 was observed to induce synthetic lethality in PARP1-deficient cells and enhanced the sensitivity of multiple cancer cells to PARP inhibitors, suggesting a role in HR down-regulation. Mechanistically, UNI66 was found to interact with and inhibit BRD4 protein binding to the promoters of CtIP and RAD51 genes, resulting in the down-regulation of their transcription. This decrease in CtIP and RAD51 expression was associated with reduced HR activity, thereby increasing the sensitivity of tumors to PARP inhibitors. These findings indicate that BRD4-mediated transcriptional regulation of CtIP and RAD51 influences HR activity, which may have implications for overcoming resistance to PARP inhibitors.

Hesperetin, a flavonoid predominantly present in citrus fruits, exhibits significant intervention effects on both the initiation and progression of gastric cancer. However, the specific mechanisms underlying this effect remain unclear.

Ovarian cancer (OC) often presents at advanced stages with poor prognosis. Although poly(ADP-ribose) polymerase inhibitors (PARPi) offer clinical benefits, resistance remains a major challenge. This study investigates the role of KLF5 in regulating OC cell stemness and contributing to PARPi resistance.

The ATP-binding cassette (ABC) transporter family is one of the largest and oldest protein families and encodes a class of transmembrane transporter proteins that transport substances in living organisms. Panax ginseng is a traditional Chinese herbal medicine, and its main active ingredient is ginsenoside, a secondary metabolite. Transportation and accumulation of secondary metabolites require the participation of ABC transporter proteins. In this study, we performed a genome-wide identification and expression analysis of the ginseng ABC transporter family using bioinformatics tools. Analysis of 106 PgABC genes showed that they were classified into seven subfamilies, among which ABCG was the most abundant subfamily. Chromosomal localization and covariance analyses showed that PgABC genes were unevenly distributed on chromosomes and that tandem repeat sequences existed. Tissue expression analyses revealed that PgABC expression was tissue-specific in ginseng. Cis-acting element analyses showed that PgABC genes responded to induction by hormones such as methyl jasmonate (MeJA). Subsequent qRT-PCR analysis of MeJA-treated ginseng adventitious roots revealed dynamic expression changes in nine PgABC genes, with PgABC14, PgABC18, and PgABC24-01 showing significant upregulation. The identification and analysis of the ABC transporter family in ginseng lays a theoretical foundation for the subsequent study of the function of the ABC gene family in ginseng and provides a theoretical basis for the study of ABC transporter proteins in other medicinal plant species.

Beta-hemoglobinopathies such as beta-thalassemia and sickle cell disease are severe genetic blood disorders affecting the beta globin chain of haemoglobin A (α2β2). Activation of delta globin, the non-alpha globin of HbA2 (α2δ2), could represent a possible approach to improve the clinical severity of these pathologies. Notably, the therapeutic potential of delta globin has been demonstrated in previous studies using a mouse model of beta-thalassemia and sickle cell disease. The present study evaluated delta globin gene activation by small molecules in erythroid cells isolated from transgenic murine foetal liver. A screening of 119 molecules, selected for their potential in drug repurposing, was performed without prior selection based on specific pathways of interest. Three candidates-Nexturastat, Stattic and Palbociclib-were found to have high efficacy on delta globin expression. Palbociclib also proved effective in increasing gamma globin expression. All of these compounds have pharmacokinetic profiles that are beneficial for clinical application, providing potential inducer agents of HbA2 that could have therapeutic effects in the treatment of beta-hemoglobinopathies.

Silicon application at a concentration of 2 mM induced sugarcane resistance to Nigrospora oryzae by upregulating pathogen recognition and defense genes, thus increasing plant metabolic activities and productivity. Sugarcane is an important global food and industrial crop, but numerous pathogens threaten its productivity. Our team recently identified the fungus Nigrospora oryzae as a pathogen affecting sugarcane's growth and productivity. Although silicon supplementation is active against most fungi, it remains unclear if it would enhance the resilience of sugarcane to N. oryzae, and molecular mechanisms underlying this process are yet to be explored. In this study, we explored the effects of four silicon concentrations (control, 1 mM, 2 mM, and 4 mM) on the growth and disease resistance of seedlings of the sugarcane variety ROC22 under fungal stress. Employing an integrative approach combining detailed phenotypic analysis with transcriptomic and metabolomic profiling, we elucidated the underlying molecular mechanisms of silicon's protective effects. Results indicated that optimal concentrations (2 mM) of silicon enhanced disease resistance and significantly improved plant height, root characteristics, and enzymatic activities. Transcriptomic analysis revealed an upregulation of genes (826) involved in pathogen recognition and defensive response, while metabolomic analysis highlighted alterations in metabolic pathways pertinent to stress response. These findings suggest that silicon supplementation could effectively bolster sugarcane's defense against fungal diseases, offering new insights into its role in plant pathology and paving the way for developing more resilient crop varieties.

MhIDA small peptides promote apple root growth by enhancing auxin synthesis and cell wall remodeling gene expression, revealing a peptide-based strategy to improve root architecture. Although small peptides have been well documented as crucial regulators of plant growth and development, the molecular mechanisms underlying lateral root morphogenesis in Malus hupehensis remain poorly understood. In this research, exogenous application of 1 µM MhIDA-Like family peptides increased primary root (PR) length by 14.31-19.96% and lateral root (LR) number by 124.54-149.08%. MhIDA, predominant expression in the root tip and lateral root primordium, demonstrated the most substantial promoting effects on PR elongation, LR number and density when the treatment concentration reached 1 µM. Furthermore, similar effects were found in MhIDA-overexpression transgenic apple seedlings, with the number and density of transgenic LRs increase by 80.52 and 126.86%, respectively, compared with wild-type seedlings. More importantly, 1 µM MhIDA treatment induced significant hormonal alterations, with the content of auxin, salicylic acid and gibberellic acid increasing by 1.5-fold, 1.4-fold, and 2.1-fold, respectively, compared to control. The qRT-PCR results showed that MhIDA could induce the expression of auxin synthesis genes (MhTAA1 and MhYUCC1) that were up-regulated by about twofold, and the cell wall remodeling-related genes (MhEXP17, MhXTR6, MhPGAZAT and MhPGLR) were upregulated by about 2- to 4-fold after 1 µM MhIDA treatment, thereby regulating LR emergence and formation of Malus hupehensis. Overall, these findings suggested the MhIDA peptide can promote the growth and development of roots, laying the foundation for cultivating apple rootstocks with strong roots and higher resistance to abiotic stress.

The peroxiredoxin (PRDX) family, also known as the peroxidase family, consists of six members that participate in a variety of essential bio-processes in carcinogenesis. However, their molecular role in lung adenocarcinoma (LUAD) has not been systematically explored. Using bioinformatic tools, we systematically analyzed the expression, prognostic value and drug sensitivity of the PRDX gene family members in LUAD. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to verify the expression of PRDX1 in both LUAD tissues and cells. Cell Counting Kit-8 (CCK-8) assay was applied to detect the half-maximal inhibitory concentration (IC50) of osimertinib in LUAD. A series of cellular drug assays, including 5-Ethynyl-2'-deoxyuridine (EdU), colony formation, and apoptosis assays, were performed to explore the correlation of PRDX1 with epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) sensitivity by using EGFR-mutant and wild-type LUAD cell lines. Among all the PRDX family members, PRDX1 has a promising prognostic value and is associated with EGFR mutations, as verified by experiments conducted on collected LUAD specimens. In addition, pathway enrichment analysis suggested that PRDX1 expression positively correlated with DNA repair, which is often considered to be inextricably linked to drug resistance in tumor cells. Thus, we validated the correlation between PRDX1 and EGFR-TKI sensitivity through a series of in vitro experiments and found that PRDX1 inhibition along with osimertinib treatment resulted in synergistic inhibition of tumor growth. Moreover, we found that PRDX1 was negatively correlated with the immune infiltration of dendritic cells (DCs) in the tumor microenvironment (TME) of LUAD, further suggesting an oncogenic role of PRDX1. This study demonstrates that high PRDX1 expression could be a potential diagnostic and prognostic marker of LUAD, and the strategy of PRDX1 knockdown provides new insights into improving the therapeutic sensitivity of EGFR-TKI in patients with LUAD.

Chemotherapeutic drugs, like cisplatin, function by damaging genomic DNA, thus inducing cell apoptosis. Cancer cells can enhance their DNA repair capacity, leading to chemotherapeutic resistance. Nucleotide excision repair (NER) involves repairing DNA adducts and crosslinks caused by chemotherapeutic agents. Transforming growth factor-beta (TGF-β) pathway contributes to carcinogenesis, DNA repair alteration, and chemoresistance. However, the connection between TGF-β pathway, NER function alteration, and resistance to cisplatin therapy remains elusive. Therefore, the objective of current study was to fill this gap by assessing the impact of TGF-β inhibition and activation on cisplatin-induced antiproliferation, apoptosis, and DNA damage using the MTT assay, flow cytometry analysis, and COMET assay, respectively. Four NER genes, XPA, XPB, XPC, and XPF, were measured using Real-time Polymerase Chain Reaction (qPCR). MDA-MB-231 cell line was utilized as a model of breast cancer. Blockade of the TGF-β pathway strengthened cisplatin cytotoxicity, whereas induction of the TGF-β pathway suppressed cisplatin cytotoxicity. In cisplatin-treated breast cancer cells, DNA damage significantly increased upon the TGF-β pathway inhibition. Conversely, cisplatin-induced DNA damage decreased significantly upon TGF-β pathway stimulation. Finally, cisplatin caused an overexpression of the four NER genes which was curtailed and augmented by TGF-β inhibition and stimulation, respectively. Overall, this study presented evidence of the impact exerted by TGF-β pathway on NER and cisplatin sensitivity of breast cancer cells.

Background: Doxorubicin (DOX) is a widely employed chemotherapeutic drug, while its clinical use is limited by the lethal cardiotoxicity. Previous studies highlighted the critical role of cardiomyocyte ferroptosis in the pathogenesis of DOX-induced cardiotoxicity (DIC). Androgen-induced gene 1 (AIG1) is perceived as a key regulator of oxidative stress-mediated cell death. Nonetheless, it remains elusive whether AIG1 is involved in the progression of DOX-induced cardiomyocyte ferroptosis and cardiotoxicity. Methods: C57BL/6 male mice were repeatedly administrated with DOX at an accumulative dosage of 20 mg/kg to establish a chronic DIC model. Global AIG1 knockout mice and AAV9-mediated cardiac-specific AIG1 knockdown or overexpression mice were utilized to evaluate the precise role of AIG1 in DIC. Additionally, the effects of AIG1 on cardiomyocyte ferroptosis were further investigated following DOX stimulation. Results: Ferroptosis played a pivotal role in DIC in both in vivo and in vitro settings. DOX exposure significantly reduced AIG1 expression levels in cardiomyocytes. Global AIG1 knockout or cardiac-specific AIG1 knockdown mice exhibited deteriorated cardiac function, adverse cardiac remodeling following DOX insult. Moreover, AIG1 deficiency aggravated DOX-evoked ferroptosis and oxidative stress in cardiomyocytes, whereas cardiac-specific overexpression of AIG1 conferred the protective effects manifested by the inhibition of cardiomyocyte ferroptosis and improvements in cardiac performance and remodeling under DOX challenge. Mechanistically, AIG1 directly interacted with the Pirh2 E3 ubiquitin ligase to promote the ubiquitination of p53, a key protein governing ferroptosis during DIC, thereby accelerating its degradation. Cardiac-specific Pirh2 knockdown markedly exacerbated DOX-induced ferroptosis by enhancing p53 activity in cardiomyocytes. Furthermore, the pharmacological administration of a highly selective p53 inhibitor PFT-α effectively ameliorated DIC in mice by inhibiting cardiomyocyte ferroptosis and substantially abrogated the deleterious cardiac effects associated with AIG knockout under DOX challenge. Conclusion: Our findings defined the critical cardioprotective role of AIG1 in DIC by alleviating cardiomyocyte ferroptosis in a Pirh2/p53 axis-dependent manner. Targeting the novelly identified AIG1-Pirh2-p53 signaling axis presents a promising approach to prevent DIC.

Retinoblastoma (Rb) is a rare cancer, yet it is the most common eye tumor in children. It can occur in either a familial or sporadic form, with the sporadic variant being more prevalent, though its downstream effects on epigenetic markers remain largely unclear. Currently, the treatment for retinoblastoma typically involves aggressive chemotherapy and surgical resection. The identification of specific epigenetic characteristics of non-hereditary (sporadic) Rb has led to the development of advanced, high-throughput methods to explore its epigenetic profile. Our previous research demonstrated that treatment with the demethylating agent 5-Aza-2'-deoxycytidine (decitabine; DAC) induced cell cycle arrest and apoptosis in a well-characterized retinoblastoma model (WERI-Rb-1). Our analysis of time-dependent gene expression in WERI-Rb-1 cells following DAC exposure has led to the development of testable hypotheses to further investigate the epigenetic impact on the initiation and progression of retinoblastoma tumors.

Gestational exposure to chemicals has been reported to transmit epigenetic modifications of germ cells not only to somatic cells but also to the germ cells of the next generation, resulting in adverse effects. Arsenic is one of the environmental chemicals of greatest concern, but it is not precisely clarified whether and how epigenetic modifications of F1 sperm caused by gestational exposure are transmitted to the next generation of somatic cells and germ cells. In the present study, we examined the effects of arsenic exposure during gestation on DNA methylation in germ line and somatic cells of the F2. The DNA methylome of F2 sperm was analyzed by reduced representation bisulfite sequencing (RRBS) and compared to that of F2 liver and testis. We found that F2 liver and testis DNA from the arsenic group exhibited the decrease in global DNA methylation levels and bias of DMC distribution toward hypoDMC observed in F1 sperm DNA which we have previously reported, but F2 sperm DNA did not exhibit those characteristics. These studies suggest that the characteristics of epigenetic modifications in F1 sperm induced by gestational arsenic exposure are reestablished in F2 somatic cells but not in F2 germ cells.

Purple sweet potato (PSP) (Ipomoea batatas (L.) Lam) is a nutrient-rich "K-favoring" crop. The reasonable application of potassium is an important means of improving the quality and yield of PSP. We designed four different forms of potassium fertilizer treatments: K2SO4, KCl, KH2PO4, and K2HPO4, and used qRT-PCR and HPLC techniques to explore their differences in anthocyanin synthesis, accumulation, quality, and yield in PSP tubers. Our findings indicate that potassium fertilizer treatment enhances the expression of structural genes such as CHI (chalcone--flavonone isomerase), F3H (naringenin,2-oxogluturate 3-dioxygenase-like), F3‧H (flavonoid 3'-monooxygenase), ANS (leucoanthocyanidin dioxygenase-like), DFR (dihydroflavonol 4-reductase-like), and CHS (chalcone synthase), which encode key enzymes of the anthocyanin metabolism pathway. This is achieved by stimulating the high levels of expression of the transcription factor MYB, which controls anthocyanin accumulation. Consequently, this leads to increased activities of key anthocyanin biosynthetic enzymes Phenylalanine ammonia lyase (PAL, EC 4.3.1.5), chalcone isomerase (CHI, EC 5.5.1.6), dihydroflavonol 4-reductase (DFR, EC 1.1.1.219), and UDP-galactose flavonoid 3-O-galactosyltransferase (UFGT, EC 2.4.1.234), thereby promoting the synthesis and accumulation of anthocyanins within PSP tubers. This ultimately improves tuber quality and yield. Analysis conducted through hierarchical clustering heat map, principal component analysis (PCA), and comprehensive evaluation revealed that PSP exhibits varying sensitivities to different forms of potassium fertilizer, with KCl treatment significantly enhancing anthocyanin production efficiency. Our results will provide a theoretical basis and data support for the rational selection of potassium fertilizer types for actual PSP production.

Chromium (Cr) and salt stresses restrict wheat growth and yield globally. Wheat crops are also adversely affected by bacterial leaf blight and stripe rust caused by Pseudomonas syringae pv. syringae (Pss) and Puccinia striiformis f. sp. tritici (Pst), respectively. WRKY transcription factors revealed great potential in elevating crop resistance to environmental factors. This study assessed the roles of Arabidopsis WRKY30 (AtWRKY30) in regulating wheat tolerance to Cr toxicity, salt stress, bacterial leaf blight and stripe rust. Wild-type and AtWRKY30-overexpressing wheat plants were exposed to non-stressful conditions, Cr toxicity (0.5 mM K2Cr2O7), salt stress (150 mM NaCl), and pathogen infections (Pss or Pst). The results indicated that Cr and salt stresses restricted the growth and reduced the level of chlorophyll, gas exchange rates and potassium content in wheat plants. However, under Cr and salt toxicity, AtWRKY30 overexpression in wheat significantly reduced the levels of oxidative stress biomarkers and minerals (Cr, sodium, and chloride), augmented the growth and yield components, and enhanced the levels of chlorophyll, potassium, gas exchange, osmoprotectants, enzymatic antioxidants, redox components, and expression of stress-related genes compared to wild-type plants. AtWRKY30 overexpression also significantly reduced bacterial leaf blight and stripe rust symptoms in wheat plants infected with Pss and Pst, respectively. Overall, this research demonstrated the effective roles of AtWRKY30 in enhancing wheat tolerance to Cr toxicity, salinity, bacterial leaf blight and stripe rust, indicating its general effect on stress tolerance and redox regulation. Hence, AtWRKY30 can be employed as a promising candidate gene to further boost crop stress tolerance.