ArticleHuman cell2025
The miR-1305/KLF5 negative regulatory loop affects pancreatic cancer cell proliferation and apoptosis.
Article in Human cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
3 citing papers in PubMed.
- KLF family of proteins in gastrointestinal tumors (Review).Oncology letters · 2026Review
- Multi-scale systems toxicology defines a KLF5-centered adverse outcome pathway linking DEHP exposure to pancreatic cancer progression and signaling programs relevant to therapy tolerance.Frontiers in cell and developmental biology · 2026Article
- HERVH-derived eRNA activates a super-enhancer-driven ALDH1A3/SAT1 axis to promote ferroptosis escape and pancreatic cancer development.Science advances · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
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.
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Registered trials
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