The divergent loop structures of nicotinic acetylcholine receptor (nAChR) α3, α5, and α7 subunits (encoded by CHRNA3, CHRNA5, and CHRNA7) are involved in kinase phosphorylation and signal transduction, potentially affecting oral squamous cell carcinoma (OSCC), the most common head and neck cancer (HNC). However, their specific roles in OSCC remain unclear.

The present study aimed to investigate the effect of microRNA (miR)-199a-3p on the biological function of non-small cell lung cancer (NSCLC) adenocarcinoma cells by targeting the fat mass and obesity‑associated protein (FTO)/myeloid zinc finger 1 (MZF1)/claudin domain‑containing 1 (CLDND1) axis. Human NSCLC cell lines, primarily A549 cells, were used for in vitro assays. Reverse transcription‑quantitative PCR and western blotting were performed to assess the expression of relevant genes and proteins. Dual‑luciferase reporter assays were used to verify the relationship between miR‑199a‑3p and FTO, as well as the transcriptional regulation of CLDND1 by MZF1. Methylated RNA immunoprecipitation was used to evaluate the N6‑methyladenosine (m6A) modification levels of MZF1, whereas photoactivatable ribonucleoside‑enhanced crosslinking and immunoprecipitation supported the binding of FTO to MZF1 mRNA. Cell proliferation, migration, invasion and apoptosis were assessed using Cell Counting Kit‑8, Transwell and flow cytometry assays. miR‑199a‑3p was downregulated in NSCLC tissues and cells. Overexpression of miR‑199a‑3p inhibited A549 cell proliferation, invasion and migration. Mechanistically, miR‑199a‑3p directly targeted and suppressed FTO, an m6A demethylase, leading to enhanced m6A modification of MZF1 mRNA and a subsequent decrease in MZF1 expression. Knockdown of MZF1 attenuated the oncogenic effects mediated by FTO, confirming that MZF1 served as a downstream effector of the miR‑199a‑3p/FTO axis. Moreover, MZF1 transcriptionally activated CLDND1, thereby facilitating the malignant phenotype of NSCLC cells. Collectively, these findings demonstrate that miR‑199a‑3p suppresses NSCLC progression by targeting FTO, promoting m6A methylation‑dependent downregulation of MZF1, and consequently decreasing CLDND1 expression. Thus, the miR‑199a‑3p/FTO/MZF1/CLDND1 axis may serve as a promising therapeutic target in NSCLC.

A highly efficient siRNA vector (PFS-CA) capable of selectively silencing genes in cancer cells was obtained by modifying common low-molecular-weight (LMW) polyethylenimine (PEI) with a bioreducible targeted multifunctional module (FS) to get PFS, followed by noncovalently incorporating chlorogenic acid (CA). FS combined folate receptor-mediated targeting for cancer cells with glutathione (GSH)-responsive siRNA release into the cytoplasm. CA, a highly biocompatible natural polyphenol served as a siRNA condensation enhancer, siRNA stabilizer, and ROS scavenger. Consequently, by the synergistic effects between PFS and CA, PFS-CA performs very well on several crucial siRNA delivery processes, including siRNA condensation, complex stability, cell uptake, endosome escape, and siRNA cytoplasmic release. The representative PFS4-3CA exhibited superior transfection efficiency in a variety of cancer cell lines, including neurogenic tumor-related PC12 cells, than commercial PEI25k and Lipo2k, and extremely high and selective gene silencing effects in cancer cells (with a gene silencing rate of 98.6% in HepG2 while only 8.4% in HK-2). Our findings demonstrated great promise for the development of a safe and effective siRNA carrier for future applications in tumor-targeted siRNA therapy.

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that the first two lanes of the Actin blot in Fig. 1D looked strikingly similar to the Actin panels in Fig. 2E for the MDA‑MB‑231 cell line, In addition, the Actin panel in Fig. 4A (showing a time series) looked very similar to the Actin panel in Fig. 4B (showing different treatments). Upon analyzing the data independently in the Editorial Office, it came to light that there was an overlapping pair of data panels for the immunohistochemical data shown in Fig. 6C, such that data which were intended to show the results from differently performed experiments appeared to have been derived from the same original source, and data featured in Fig. 6D had subsequently appeared in a paper published in the journal Tumor Biology that was written by different authors at different research institutes. The authors were contacted by the Editorial Office to offer an explanation for these possible anomalies in the presentation of the data in this paper, although up to this time, no response from them has been forthcoming. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office conitnues to investigate this matter further. [International Journal of Oncology 48: 2479‑2487, 2016; DOI: 10.3892/ijo.2016.3483].

Schisantherin A (Sch A), a compound derived from Schisandra chinensis, has anti‑inflammatory, antitumor, neuroprotective and antifibrotic properties. However, to the best of our knowledge, the role of Sch A in non‑small cell lung cancer (NSCLC) has not yet been reported. The purpose of the present study was to determine whether Sch A can prevent the development of NSCLC and to elucidate the underlying mechanisms involved. The results of the present study demonstrated that Sch A inhibited the viability of A549 and HCC827 cells. Furthermore, Sch A increased the intracellular Fe2+ level, reduced the mitochondrial membrane potential and depleted the glutathione content in lung cancer cells. These effects were reversed by the ferroptosis inhibitors ferrostatin‑1 and deferoxamine. Bioinformatics analysis and reverse transcription‑quantitative PCR results suggested that Sch A increased the mRNA levels of the transcription factor yes‑associated protein (YAP). Additionally, Sch A upregulated the expression of YAP and ferroptosis‑related proteins, including acyl‑CoA synthase long‑chain family member 4 (ACSL4) and transferrin receptor (TfR), in lung cancer cells. Silencing of YAP led to the downregulation of its downstream targets, ACSL4 and TfR, even in the presence of Sch A. In vivo, Sch A significantly inhibited subcutaneous tumor growth in nude mice. In conclusion, Sch A may activate the YAP/ACSL4/TfR signaling axis to induce ferroptosis in NSCLC cells, positioning it as a potential small‑molecule therapeutic agent for NSCLC.

To assess whether miRNA expression can be a biomarker for distinguishing between hyperplastic and adenomatous polyps and colon cancer tissues.

Ovarian cancer is one of the most malignant tumors in women. Long noncoding RNAs have been demonstrated to regulate multiple biological processes, including cell proliferation, migration, apoptosis, and drug resistance, in various cancers. Small nucleolar RNA (snoRNA) host genes (SNHGs) are a group of long noncoding RNAs. Studies have reported that SNHGs are aberrantly expressed in many kinds of cancers and are associated with poor patient prognosis. In ovarian cancer, SNHGs play critical roles in the development and progression of ovarian cancer via different pathways. However, there is a lack of systematic reports on the research progress of SNHGs in ovarian cancer. Therefore, we reviewed the studies on the roles of SNHGs in the early diagnosis, development, and treatment of ovarian cancer and explored the underlying mechanisms to provide new insights into the treatment of ovarian cancer.

Breast cancer is the leading cause of cancer-related mortality in women, with triple-negative breast cancer (TNBC) being an aggressive subtype associated with poor prognosis and limited treatment options. TNBC is known for its immunogenic characteristics, including high genetic instability and elevated tumor-infiltrating lymphocytes (TILs). Immune checkpoint inhibitors (ICIs) have shown efficacy in TNBC treatment, but the optimal treatment duration in case of prolonged response remains unclear.

Ferroptosis, a regulated form of iron-dependent cell death, has shown promise as an anti-tumor mechanism. However, its role in pancreatic cancer remains largely unexplored. This study aimed to identify a ferroptosis-related prognostic signature and key biomarkers.

Extramedullary Plasmacytoma (EMP) is a rare plasma cell neoplasm that originates outside the bone marrow. Primary Extramedullary Plasmacytoma with Diffuse Lymph Node Involvement (PLNEMP) is exceptionally rare. Here, we report a unique case of PLNEMP and significant bone destruction, characterized by a novel IGH::NFKB1 fusion gene. A 60-year-old Chinese male presented with palpable enlarged lymph nodes in the left inguinal region. After completing laboratory tests and examinations, it was suggested that there was monoclonal immunoglobulinemia and multiple bone destruction. Pathological examination of the left inguinal lymph node biopsy showed plasmacytoma with monoclonal gammopathy. Genomic profiling identified a novel IGH::NFKB1 fusion gene. The two 3' regulatory region (3'RR) enhancers of the IGH locus were fused to a region 379 bp upstream of NFKB1 exon 1, resulting in overexpression of NFKB1. The patient received four cycles of chemotherapy with Mitoxantrone hydrochloride liposome (Lipo-MIT) combined with Bortezomib, Pomalidomide, and Dexamethasone (MVPD), achieving very good partial remission (VGPR) in hematological and partial remission (PR) in extramedullary disease. Subsequently, he underwent autologous stem cell transplantation (ASCT) followed by BCMA CAR-T cell therapy. At 8 months post-transplantation, complete remission (CR) was achieved in hematological parameters, and the extramedullary disease showed a response greater than PR. The patient has survived for 26 months so far. This case highlights the importance of recognizing the rare presentation of PEMP with diffuse lymph node involvement and significant bone destruction. The presence of the novel IGH::NFKB1 fusion gene provides insights into the potential role of the NF-κB pathway in the pathogenesis of this disease. The successful treatment with MVPD chemotherapy, ASCT, and BCMA CAR-T therapy demonstrates the potential efficacy of this combined therapeutic approach in achieving long-term remission and survival in such rare cases. Further studies are warranted to explore the therapeutic implications of targeting the NF-κB pathway in similar cases of EMP with bone destruction.

Colorectal cancer (CRC) is the third most common malignancy worldwide and the second leading cause of cancer-related deaths. Its progression is driven by genetic and epigenetic alterations, with increasing evidence emphasizing the role of the transcriptome, particularly post-transcriptional modifications. Human antigen R (HuR), an RNA-binding protein (RBP), plays a crucial role in post-transcriptional regulation of gene expression. In the context of tumor progression, HuR affects a range of cellular processes, including cell proliferation, survival, and metabolic reprogramming, via regulating target mRNA stability and translation. Additionally, HuR influences the tumor microenvironment (TME) through modulating target mRNAs involved in inflammation, immune responses, extracellular matrix remodeling and angiogenesis. Despite these insights, the precise mechanisms by which HuR regulates post-transcriptional process in CRC remain unclear. This review first provides an overview of HuR's roles and the underlying mechanisms involved in CRC progression, including its regulation of mRNA expression, control of the cell cycle, and modulation of the TME. We also discussed the potential of HuR as a therapeutic target, exploring how targeting HuR could slow down CRC progression and metastasis, ultimately leading to more effective and personalized treatment strategies.

This study aimed to validate secreted biomarkers SPON2 and MSMB with tumor-specific expression and immunogenicity for nanomaterial-based prostate cancer diagnostics.

Hepatocellular carcinoma (HCC) lacks reliable prognostic biomarkers for immunotherapy. Immunogenic cell death (ICD) represents a promising therapeutic target, but its comprehensive characterization in HCC remains unexplored.

Acute myeloid leukemia (AML) remains a therapeutic challenge due to its high relapse rate and limited treatment options. This study aimed to identify and validate novel circulating protein biomarkers with causal roles in AML pathogenesis using an integrative multi-omics approach.

Breast cancer (BC) remains a widespread malignancy and ranks as the second leading cause of cancer-related mortality among women worldwide. Hypoxia, epithelial-mesenchymal transition (EMT), and immune-related processes have been increasingly recognized as critical contributors to BC pathogenesis. However, a prognostic model integrating hypoxia-, EMT-, and immune-related genes (HEMTIRGs) to predict BC outcomes has not yet been established.

The recent advancement of mRNA technology has opened new therapeutic avenues for treating hematologic malignancies, offering innovative approaches to enhance existing immunotherapies. This review examines the expanding role of in vitro transcribed (IVT)-mRNA-based platforms in hemato-oncology, focusing on key areas: monoclonal antibody production, bispecific antibody development, and CAR-T cell engineering. Unlike conventional biologics, mRNA allows for in vivo expression of therapeutic proteins, reducing manufacturing complexity and expanding access through scalable, cell-free synthesis. IVT-mRNA-encoded monoclonal and bispecific antibodies can overcome limitations such as short half-life and the need for continuous infusion, while enabling innovations like Fc silencing, protease-activated masking, and combinatorial immunotherapies. In CAR-T cell therapy, IVT-mRNA provides transient, safer alternatives to viral vector-based approaches and facilitates emerging strategies such as in vivo CAR programming and IVT-mRNA vaccine-like boosters. Despite these advantages, challenges remain, including delivery precision, durability of therapeutic effects, and limited clinical trial success. Beyond therapeutic mechanisms, the integration of bioinformatics and AI in IVT-mRNA design is accelerating the development of personalized and efficient cancer treatments. Overall, mRNA technology is redefining immunotherapy in hematology and holds the potential to broaden access to advanced treatments globally.

Prognostication in pediatric and young adult osteosarcoma is typically limited to metastatic status at diagnosis and tumor necrosis after chemotherapy. Despite a complex genomic landscape, few molecular biomarkers are used clinically. This study evaluates the prognostic relevance of MYC amplification and MYC protein expression.

To evaluate the efficacy, safety, and predictive biomarker of a third-generation tyrosine kinase inhibitor (3G-TKI; ponatinib or olverembatinib) combined with azacitidine in chronic myeloid leukemia (CML) in myeloid blast phase.

The relapse after chimeric antigen receptor (CAR) T-cell therapy remains a critical challenge, and the optimal timing and treatment strategies for CAR T urgently need to be explored. Autologous hematopoietic stem cell transplantation (auto-HSCT) demonstrates comparable leukemia-free survival (LFS) and overall survival (OS) in patients who rapidly achieve MRD-negative complete remission (CR) compared with allogeneic HSCT (allo-HSCT). Thus, combining CAR T cells with auto-HSCT may represent a promising treatment strategy. The trial registration is ClinicalTrials.gov identifier NCT05470777.

Chromatin regulators (CRs) play a critical role in tumorigenesis, drug response, and prognosis, with dysregulation of chromatin regulator genes (CRGs) potentially disrupting the tumor immune microenvironment (TME) and influencing immune responses in cervical cancer. However, the prognostic and therapeutic implications of integrating CRGs and TME parameters in cervical cancer remain poorly understood.