Mechanisms behind the LncRNAs-mediated regulation of paclitaxel (PTX) resistance in human malignancies

IF 3.3 3区 生物学 Q3 CELL BIOLOGY
Ali G. Alkhathami , Harikumar Pallathadka , Sejal Shah , Subbulakshmi Ganesan , Abhishek Sharma , Seema Devi , Yasser Fakri Mustafa , Mohammed Qasim Alasheqi , Abed J. Kadhim , Ahmed Hussein Zwamel
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引用次数: 0

Abstract

Paclitaxel (PTX) is extensively used to treat various cancers, including those of the breast, ovary, lung, esophagus, stomach, pancreas, and neck. However, despite its effectiveness in clinical settings, patients often experience cancer recurrence due to the emergence of resistance to PTX. The mechanisms underlying this resistance in cancer cells exposed to PTX involve modifications in β-tubulin, the primary target molecule associated with mitosis, the activation of pathways that facilitate drug efflux, and the dysregulation of apoptosis-related proteins. Long non-coding RNAs (lncRNAs), which are RNA molecules exceeding 200 nucleotides in length and lacking protein-coding capabilities, play various regulatory roles in cellular functions. A growing body of evidence underscores the role of lncRNAs in cancer progression and their involvement in PTX resistance across different cancer types. As a result, lncRNAs have been identified as promising therapeutic targets for overcoming drug resistance in cancer therapies. This review aims to provide an overview of the current knowledge regarding lncRNAs and their contributions to resistance mechanisms to promote further research in this field. A summary of key lncRNAs and their related pathways associated with PTX resistance will be presented.
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来源期刊
Experimental cell research
Experimental cell research 医学-细胞生物学
CiteScore
7.20
自引率
0.00%
发文量
295
审稿时长
30 days
期刊介绍: Our scope includes but is not limited to areas such as: Chromosome biology; Chromatin and epigenetics; DNA repair; Gene regulation; Nuclear import-export; RNA processing; Non-coding RNAs; Organelle biology; The cytoskeleton; Intracellular trafficking; Cell-cell and cell-matrix interactions; Cell motility and migration; Cell proliferation; Cellular differentiation; Signal transduction; Programmed cell death.
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