miR-630 as a therapeutic target in pancreatic cancer stem cells: modulation of the PRKCI-Hedgehog signaling axis.

IF 5.7 2区生物学 Q1 BIOLOGY

Biology Direct Pub Date : 2024-11-11 DOI:10.1186/s13062-024-00539-1

Jun Zou, Sha Yang, Chongwu He, Lei Deng, Bangran Xu, Shuai Chen

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引用次数: 0

Abstract

Background: MicroRNAs (miRNAs) are critical regulators of cancer progression, prompting our investigation into the specific function of miR-630 in pancreatic cancer stem cells (PCSCs). Analysis of miRNA and mRNA expression data in PCSCs revealed downregulation of miR-630 and upregulation of PRKCI, implying a potential role for miR-630 in PCSC function and tumorigenicity.

Results: Functional assays confirmed that miR-630 directly targets PRKCI, leading to the suppression of the Hedgehog signaling pathway and consequent inhibition of PCSC self-renewal and tumorigenicity in murine models. This study unveiled the modulation of the PRKCI-Hedgehog signaling axis by miR-630, highlighting its promising therapeutic potential for pancreatic cancer (PC) treatment.

Conclusions: MiR-630 emerges as a pivotal regulator in PCSC biology, opening up new avenues for targeted interventions in PC. The inhibitory effect of miR-630 on PCSC behavior underscores its potential as a valuable therapeutic target, offering insights into innovative treatment strategies for this challenging disease.

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作为胰腺癌干细胞治疗靶点的 miR-630：PRKCI-Hedgehog 信号轴的调节。

背景：微RNA（miRNA）是癌症进展的关键调控因子，这促使我们研究miR-630在胰腺癌干细胞（PCSCs）中的特殊功能。对PCSCs中miRNA和mRNA表达数据的分析表明，miR-630下调，PRKCI上调，这意味着miR-630在PCSC的功能和致瘤性中可能发挥作用：功能测定证实，miR-630直接靶向PRKCI，导致Hedgehog信号通路受到抑制，从而抑制了小鼠模型中PCSC的自我更新和致瘤性。这项研究揭示了miR-630对PRKCI-Hedgehog信号轴的调控作用，凸显了其在胰腺癌（PC）治疗中的巨大潜力：结论：miR-630是胰腺癌细胞生物学的关键调控因子，为靶向干预胰腺癌开辟了新途径。miR-630对PCSC行为的抑制作用凸显了其作为有价值的治疗靶点的潜力，为这一具有挑战性的疾病的创新治疗策略提供了启示。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Biology Direct 生物-生物学

CiteScore

6.40

自引率

10.90%

发文量

审稿时长

7 months

期刊介绍： Biology Direct serves the life science research community as an open access, peer-reviewed online journal, providing authors and readers with an alternative to the traditional model of peer review. Biology Direct considers original research articles, hypotheses, comments, discovery notes and reviews in subject areas currently identified as those most conducive to the open review approach, primarily those with a significant non-experimental component.