Insight into the molecular mechanisms of gastric cancer stem cell in drug resistance of gastric cancer

Xiong, Jixian; Zhang, Tiantian; Lan, Penglin; Zhang, Shuhong; Fu, Li

doi:10.20517/cdr.2022.11

Cited by 5 publications

(2 citation statements)

References 167 publications

(229 reference statements)

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Section: Introductionmentioning

confidence: 99%

“…6,7 Identifying the molecular mechanisms that lead to the progression and metastasis of GC tumors is crucial in developing practical therapeutic approaches for treating this malignancy. 8 Accumulating investigations have indicated that besides genetic and epigenetic mechanisms, microRNAs (miRNAs) may regulate various biological processes and be significant modulators of tumorigenesis in different cancers, including GC, through post-transcriptional regulation of tumor suppressors and oncogenes. 2,9 miRNAs are a group of endogenous non-coding and regulatory RNAs with an estimated length of 18-22 nucleotides that play an important role in the negative regulation of gene expression, mainly by binding to the 3'UTR regions of the target mRNAs and occlusion of their translation.…”

Section: Introductionmentioning

confidence: 99%

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Simultaneous suppression of miR-21 and restoration of miR-145 in gastric cancer cells; a promising strategy for inhibition of cell proliferation and migration

Bilan,

Amini,

Doustvandi

et al. 2023

Bioimpacts

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Introduction: Around the world, gastric cancer (GC) is the third leading cause of cancer-related deaths. microRNAs are a group of regulatory non-coding RNAs that are involved in GC progression. miR-145 as a tumor suppressor and miR-21 as an oncomiR were shown to be dysregulated in many cancers, including GC. This research aimed to enhance the expression of miR-145 while reducing the expression of miR-21 and examine their impact on the proliferation, apoptosis, and migration of GC cells. Methods: KATO III cells with high expression levels of miR-21-5p and low expression of miR-145-5p were selected. These cells were then transfected with either miR-145-5p mimics or anti-miR-21-5p, alone or in combination. Afterward, the cell survival rate was determined using the MTT assay, while apoptosis induction was investigated through V-FITC/PI and DAPI staining. Additionally, cell migration was examined using the wound healing assay, and cell cycle progression was analyzed through flow cytometry. Furthermore, gene expression levels were quantified utilizing the qRT-PCR technique. Results: The study's findings indicated that the co-replacement of miR-145-5p and anti-miR-21-5p led to a decrease in cell viability and the induction of apoptosis in GC cells. This was achieved via modulating the expression of Bax and Bcl-2, major cell survival regulators. Additionally, the combination therapy significantly increased sub-G1 cell cycle arrest and reduced cell migration by downregulating MMP-9 expression as an epithelial-mesenchymal transition marker. This study provides evidence for the therapeutic possibility of the combination of miR-145-5p and anti-miR-21-5p and also suggests that they could inhibit cell proliferation by modulating the PTEN/AKT1 signaling pathway. Conclusions: Our research revealed that utilizing miR-145-5p and anti-miR-21-5p together could be a promising therapeutic approach for treating GC.

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Section: Introductionmentioning

confidence: 99%