miRNA regulation of the Akt/mTOR pathway in oral squamous cell carcinoma: a focused review.

IF 2.9 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM
Shazia Fathima Jaffer Hussain, Mohammad Fareed, Mohmed Isaqali Karobari
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引用次数: 0

Abstract

Oral squamous cell carcinoma (OSCC) contributes significantly to global cancer mortality, characterized by a progression from hyperplasia to invasive cancer through a series of genetic and epigenetic alterations. Central to this progression is the Akt/mTOR signaling pathway, which regulates cell proliferation and survival. This review examines the role of microRNAs (miRNAs) in modulating the Akt/mTOR pathway and their implications for OSCC. The Akt/mTOR pathway, activated by receptor tyrosine kinases and involving the PI3K/AKT/mTOR complexes, is crucial for tumor cell growth and metabolism. Dysregulation of this pathway is frequently observed in OSCC, leading to increased proliferation, survival, and metastasis. miRNAs, such as miR-21, miR-99, and miR-145, play significant roles in regulating this pathway by influencing key components like Akt and mTOR. These miRNAs can act as oncogenes or tumor suppressors, affecting cancer progression and response to therapy. The review highlights the potential of targeting miRNAs for OSCC treatment, including strategies to restore normal miRNA levels or inhibit aberrant miRNAs. Such targeted therapies offer promise for improving treatment outcomes and overcoming drug resistance in OSCC.

口腔鳞状细胞癌中miRNA调控Akt/mTOR通路的研究综述
口腔鳞状细胞癌(OSCC)是全球癌症死亡率的重要组成部分,其特点是通过一系列遗传和表观遗传改变从增生到浸润性癌症的进展。这一过程的核心是Akt/mTOR信号通路,它调节细胞增殖和存活。本文综述了microRNAs (miRNAs)在调节Akt/mTOR通路中的作用及其对OSCC的影响。Akt/mTOR通路由受体酪氨酸激酶激活,涉及PI3K/ Akt/mTOR复合物,对肿瘤细胞生长和代谢至关重要。在OSCC中经常观察到该通路的失调,导致增殖、存活和转移增加。miR-21、miR-99和miR-145等mirna通过影响Akt和mTOR等关键成分在调控该通路中发挥重要作用。这些mirna可以作为癌基因或肿瘤抑制因子,影响癌症的进展和对治疗的反应。该综述强调了靶向miRNA治疗OSCC的潜力,包括恢复正常miRNA水平或抑制异常miRNA的策略。这种靶向治疗为改善OSCC的治疗效果和克服耐药性提供了希望。
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
Discover. Oncology
Discover. Oncology Medicine-Endocrinology, Diabetes and Metabolism
CiteScore
2.40
自引率
9.10%
发文量
122
审稿时长
5 weeks
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