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<p>Pancreatic cancer (PC) is characterized by a high relapse rate and unfavorable prognosis. Currently, the optimal treatment for PC is complete resection followed by adjuvant systemic chemotherapy. Nevertheless, tumor cell repopulation and subsequent tumor relapse and metastasis after chemotherapy result in a poor prognosis. Therefore, it is of great value to explore the potential molecular mechanisms underlying PC for developing novel treatment strategies. Herein, we aimed to investigate the potential regulatory mechanism of miR-1305 upon aerobic proliferation, metastasis, and apoptosis in PC. miR-1305 was downregulated in PC tissues and cell lines. miR-1305 overexpression prominently inhibited PC cell proliferation and metastasis promoted cell apoptosis in vitro<i>,</i> and alleviated PC formation in vivo. As predicted, <i>KLF5</i> could directly bind to miR-1305. Silencing of <i>KLF5</i> or KLF5 inhibitor (ML264) suppressed PC cell viability and cell invasion, and enhanced cell apoptosis. <i>KLF5</i> restrained miR-1305 transcription and expression by binding to its promoter region. miR-1305 exerted a suppressive effect on PC cell proliferation and apoptosis via regulation of the <i>KLF5</i>-<i>ERBB2</i> axis; <i>KLF5</i> gene is a transcriptional regulator of miR-1305, promising to be a new target for the diagnosis and treatment of PC.</p>

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The miR-1305/KLF5 negative regulatory loop affects pancreatic cancer cell proliferation and apoptosis

  • 期刊论文

  • 发表日期：

    2025年2月8日

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  • Yufu Zhou,
  • Yulin Tang,
  • Feizhou Huang,
  • Zhichao Wang,
  • Zhengbin Wen,
  • Qi Fang,
  • Changfa Wang

摘要

Pancreatic cancer (PC) is characterized by a high relapse rate and unfavorable prognosis. Currently, the optimal treatment for PC is complete resection followed by adjuvant systemic chemotherapy. Nevertheless, tumor cell repopulation and subsequent tumor relapse and metastasis after chemotherapy result in a poor prognosis. Therefore, it is of great value to explore the potential molecular mechanisms underlying PC for developing novel treatment strategies. Herein, we aimed to investigate the potential regulatory mechanism of miR-1305 upon aerobic proliferation, metastasis, and apoptosis in PC. miR-1305 was downregulated in PC tissues and cell lines. miR-1305 overexpression prominently inhibited PC cell proliferation and metastasis promoted cell apoptosis in vitro, and alleviated PC formation in vivo. As predicted, KLF5 could directly bind to miR-1305. Silencing of KLF5 or KLF5 inhibitor (ML264) suppressed PC cell viability and cell invasion, and enhanced cell apoptosis. KLF5 restrained miR-1305 transcription and expression by binding to its promoter region. miR-1305 exerted a suppressive effect on PC cell proliferation and apoptosis via regulation of the KLF5-ERBB2 axis; KLF5 gene is a transcriptional regulator of miR-1305, promising to be a new target for the diagnosis and treatment of PC.