The role of excision repair cross-complementation group 6-like (ERCC6L) has been reported in several cancers, but little is known about its expression and function in laryngeal squamous cell carcinoma (LSCC). In this study, the expression of ERCC6L in LSCC was determined by immunohistochemistry and its correlation with prognostic factors was analyzed. Furthermore, cytological functional validation elucidated the role and underlying mechanisms of ERCC6L dysregulation in LSCC. Our data revealed that ERCC6L expression was elevated in LSCC and it's correlated with TNM stage. In addition, ERCC6L knockdown LSCC cells showed decreased proliferation and migration, increased apoptosis, and reactive oxygen species (ROS). Mechanically, overexpression of ERCC6L promoted nuclear translocation of FOXM1 to facilitate direct binding to the KIF4A promoter and upregulated KIF4A expression. Furthermore, KIF4A knockdown attenuated the role of ERCC6L overexpression in promoting proliferation, migration, and tumorigenesis of LSCC cells. In summary, ERCC6L promoted the binding of FOXM1 and KIF4A in LSCC cells to drive their progression, which may be a promising target for precision therapy in this disease.
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http://dx.doi.org/10.1038/s41420-023-01314-3 | DOI Listing |
Nat Commun
January 2025
Jiangsu Provincial Key Laboratory of Geriatrics, Department of Geriatrics, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Immune functions decline with aging, leading to increased susceptibility to various diseases including tumors. Exploring aging-related molecular targets in elderly patients with cancer is thus highly sought after. Here we find that an ER transmembrane enzyme, sterol O-acyltransferase 2 (SOAT2), is overexpressed in regulatory T (Treg) cells from elderly patients with lung squamous cell carcinoma (LSCC), while radiomics analysis of LSCC patients associates increased SOAT2 expression with reduced immune infiltration and poor prognosis.
View Article and Find Full Text PDFGene
January 2025
Department of Otolaryngology Head and Neck Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Object: N6-methyladenosine (mA), is well known as the most abundant epigenetic modification in messenger RNA, but its influence on laryngeal squamous cell carcinoma (LSCC) remains largely unexplored and poorly understood. This study was designed to explore the effects of mA on WISP1-mediated epithelial-mesenchymal transition (EMT) and tumorigenesis in LSCC.
Methods: mA methylated and expression levels of WISP1 in LSCC tumor tissues and cells were measured by MeRIP-qPCR, qRT-PCR, and western blotting.
Cancer Cell Int
January 2025
Department of Otolaryngology, Pudong Gongli Hospital, Shanghai, 200135, China.
Background: Specific molecular mechanisms by which AURKA promoted LSCC metastasis were still unknown.
Methods: Bioinformatic analysis was performed the relationship between TRIM28 and LSCC. Immunohistochemistry, Co-IP assay, Rt-PCR and Western Blot were used to examine the expression of related molecular.
Cancer Immunol Immunother
January 2025
Department of Otorhinolaryngology-Head and Neck Surgery, The Second Affiliated Hospital of Harbin Medical University, No. 246 Xuefu Road, Nangang District, Harbin, 150001, Heilongjiang Province, China.
Background: Tumor-derived small extracellular vesicles (sEVs) play an essential role in reprogramming the tumor microenvironment. Metabolic reprogramming is an essential prerequisite for M2 polarization of tumor-associated macrophages (TAMs). This M2 phenotype is closely related to the immune dysfunction of CD8 T cells and subsequent tumor progression.
View Article and Find Full Text PDFOncol Rep
February 2025
Department of Otolaryngology Head & Neck Surgery, The First Hospital, Shanxi Medical University, Taiyuan, Shanxi 030001, P.R. China.
Laryngeal squamous cell carcinoma (LSCC), which represents a significant proportion of head and neck squamous cell carcinoma cases, is often diagnosed at advanced stages, underscoring the urgent need for effective biomarkers and therapeutic targets. Junctional adhesion molecule 3 () is implicated in various types of cancer; however, its role in LSCC remains unclear. Therefore, the present study aimed to investigate the epigenetic regulation and tumor‑suppressive functions and mechanisms of in LSCC.
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