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<p>Gastric cancer (GC) is a prevalent malignancy and one of the leading causes of cancer-related mortality worldwide. The role of transmembrane channel-like 5 (TMC5) in GC remains unknown. In this study, we analyzed the expression of TMC5 in GC using a multi-faceted approach, including analysis of public databases, immunohistochemical assays, and Western blot analyses. Our results demonstrated that TMC5 was overexpressed in GC tissues and cell lines, which was associated with poor prognosis and various clinical characteristics. We observed that the mutation rates of TMC5 in GC were low, and its methylation status was inversely related to its expression levels. Furthermore, functional assays demonstrated that TMC5 promoted GC cell proliferation, migration, and invasion in vitro, as well as tumor growth and metastasis in vivo. Furthermore, the TMC5 expression level was positively correlated with stemness and chemotherapy resistance in GC. Additionally, TMC5 was associated with multiple immune cell infiltration levels, immunotherapy response and immune checkpoint genes. Subsequently, the co-expression genes of TMC5 in GC were screened and verified by qRT-PCR. Gene set enrichment analysis showed that these genes were mainly involved in biosynthesis, metabolic pathways, and multiple classic cancer-related signaling pathways. In conclusion, our study reveals the important role of TMC5 in GC and provides potential new targets and strategies for the diagnosis and treatment of GC.</p>

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The expression of transmembrane channel-like 5 in gastric cancer and its impact on tumor progression

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年8月25日

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  • Yucai Wei,
  • Jiaxing Zhang,
  • Xiaomei Li,
  • Weijing Zhu,
  • Peng Zhang,
  • Huijuan Cheng,
  • Qian Chen,
  • Zhongjie Wen,
  • Huanhuan Liu,
  • Lei Zhao,
  • Yumin Li

摘要

Gastric cancer (GC) is a prevalent malignancy and one of the leading causes of cancer-related mortality worldwide. The role of transmembrane channel-like 5 (TMC5) in GC remains unknown. In this study, we analyzed the expression of TMC5 in GC using a multi-faceted approach, including analysis of public databases, immunohistochemical assays, and Western blot analyses. Our results demonstrated that TMC5 was overexpressed in GC tissues and cell lines, which was associated with poor prognosis and various clinical characteristics. We observed that the mutation rates of TMC5 in GC were low, and its methylation status was inversely related to its expression levels. Furthermore, functional assays demonstrated that TMC5 promoted GC cell proliferation, migration, and invasion in vitro, as well as tumor growth and metastasis in vivo. Furthermore, the TMC5 expression level was positively correlated with stemness and chemotherapy resistance in GC. Additionally, TMC5 was associated with multiple immune cell infiltration levels, immunotherapy response and immune checkpoint genes. Subsequently, the co-expression genes of TMC5 in GC were screened and verified by qRT-PCR. Gene set enrichment analysis showed that these genes were mainly involved in biosynthesis, metabolic pathways, and multiple classic cancer-related signaling pathways. In conclusion, our study reveals the important role of TMC5 in GC and provides potential new targets and strategies for the diagnosis and treatment of GC.