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Review
. 2024 May 22;14(6):608.
doi: 10.3390/biom14060608.

Long Non-Coding RNAs in Drug Resistance of Gastric Cancer: Complex Mechanisms and Potential Clinical Applications

Xiangyu Meng  1   2 , Xiao Bai  1 , Angting Ke  1 , Kaiqiang Li  1 , Yun Lei  1 , Siqi Ding  1 , Dongqiu Dai  1   3
Affiliations
Review

Long Non-Coding RNAs in Drug Resistance of Gastric Cancer: Complex Mechanisms and Potential Clinical Applications

Xiangyu Meng et al. Biomolecules. .

Abstract

Gastric cancer (GC) ranks as the third most prevalent malignancy and a leading cause of cancer-related mortality worldwide. However, the majority of patients with GC are diagnosed at an advanced stage, highlighting the urgent need for effective perioperative and postoperative chemotherapy to prevent relapse and metastasis. The current treatment strategies have limited overall efficacy because of intrinsic or acquired drug resistance. Recent evidence suggests that dysregulated long non-coding RNAs (lncRNAs) play a significant role in mediating drug resistance in GC. Therefore, there is an imperative to explore novel molecular mechanisms underlying drug resistance in order to overcome this challenging issue. With advancements in deep transcriptome sequencing technology, lncRNAs-once considered transcriptional noise-have garnered widespread attention as potential regulators of carcinogenesis, including tumor cell proliferation, metastasis, and sensitivity to chemo- or radiotherapy through multiple regulatory mechanisms. In light of these findings, we aim to review the mechanisms by which lncRNAs contribute to drug therapy resistance in GC with the goal of providing new insights and breakthroughs toward overcoming this formidable obstacle.

Keywords: clinical application; drug resistance-related lncRNAs; gastric cancer; mechanisms.

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Figure 1
Figure 1
Overview and malignant phenotypes of drug resistance-related lncRNAs in GC. Zone A: Metastasis and drug resistance-related lncRNAs. Zone B: Apoptosis and drug resistance-related lncRNAs. Zone C: Proliferation and drug resistance-related lncRNAs.GC: gastric cancer.
Figure 2
Figure 2
Upstream and downstream regulation mechanisms of drug resistance-related lncRNAs. (A) Upstream regulation of drug resistance-related lncRNAs (DR: drug resistance; FAO: fatty acid oxidation). (B) Downstream regulation of drug resistance-related lncRNAs on scaffold-like lncRNAs in the nucleus and transcription/translation functions of lncRNAs in the cytoplasm. (C) Downstream regulation of drug resistance-related lncRNAs on enhancer-like lncRNAs in the nucleus (S/T: stabilize/transcribe).
Figure 3
Figure 3
Epigenetics and drug resistance-related lncRNAs including DNA methylation, histone modification, RNA m6A modification, DNA repair, and ubiquitination.
Figure 4
Figure 4
Drug resistance-related lncRNA-mediated regulation of cell signaling (DR: drug resistance; DS: drug sensitivity).
Figure 5
Figure 5
The ”cross-talk” among metabolism, tumor microenvironment, and drug resistance-related lncRNAs.
See this image and copyright information in PMC

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