Clinical crosstalk between microRNAs and gastric cancer (Review)

Ouyang, Jing; Xie, Zhizhong; Lei, Xiaoyong; Tang, Guotao; Gan, Runliang; Yang, Xiaoyan

doi:10.3892/ijo.2021.5187

Cited by 21 publications

(16 citation statements)

References 136 publications

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“…Accumulating evidence suggests that various non-coding regulatory miRNAs, including miR-27a, miR-196a-1, miR-208a and miR-206, also serve a prominent role in the activation of the Wnt/β-catenin signaling pathway by inactivating SFRP1, which induces GC cell proliferation, migration, invasion and metastasis (46,(75)(76)(77)(78)(79)(80). In addition, long non-coding RNAs (lncRNAs) are also emerging as key players in mediating this process (81).…”

Section: Discussionmentioning

confidence: 99%

Aberrant expression of SFRP1, SFRP3, DVL2 and DVL3 Wnt signaling pathway components in diffuse gastric carcinoma

et al. 2021

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Diffuse gastric carcinoma (DGC) is characterized by poorly cohesive cells, highly invasive growth patterns, poor prognosis and resistance to the majority of available systemic therapeutic strategies. It has been previously reported that the Wnt/β-catenin signaling pathway serves a prominent role in the tumorigenesis of gastric carcinoma. However, the mechanism underlying the dysregulation of this pathway in DGC has not been fully elucidated. Therefore, the present study aimed to investigate the expression profiles of Wnt antagonists, secreted frizzled-related protein 1 (SFRP1) and secreted frizzled-related protein 3 (SFRP3), and dishevelled protein family members, dishevelled segment polarity protein 2 (DVL2) and dishevelled segment polarity protein 3 (DVL3), in DGC tissues. The association between the expression levels of these factors and the clinicopathological parameters of the patients was determined. Protein and mRNA expression levels in 62 DGC tumor tissues and 62 normal gastric mucosal tissues obtained from patients with non-malignant disease were measured using immunohistochemical and reverse transcription-quantitative PCR (RT-qPCR) analysis. Significantly lower protein expression levels of SFRP1 (P<0.001) and SFRP3 (P<0.001), but significantly higher protein expression levels of DVL2 (P<0.001) and DVL3 (P<0.001) were observed in DGC tissues compared with in control tissues by immunohistochemistry. In addition, significantly lower expression levels of SFRP1 (P<0.05) and higher expression levels of DVL3 (P<0.05) were found in in DGC tissues compared with those in normal gastric mucosal tissues using RT-qPCR. According to correlation analysis between the SFRP1, SFRP3, DVL2 and DVL3 protein expression levels and the clinicopathological characteristics of patients with DGC, a statistically significant correlation was found between the SFRP3 volume density and T stage (r=0.304; P=0.017) and between the SFRP3 volume density and clinical stage (r=0.336; P=0.008). In conclusion, the findings of the present study suggested that the Wnt signaling pathway components SFRP1, SFRP3, DVL2 and DVL3 may be aberrantly expressed in DGC tissues, implicating their possible role in the development of this malignant disease. The present data also revealed a positive relationship between SFRP3 protein expression and the clinical and T stage of DGC.

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Section: Discussionmentioning

confidence: 99%

Aberrant expression of SFRP1, SFRP3, DVL2 and DVL3 Wnt signaling pathway components in diffuse gastric carcinoma

et al. 2021

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“…MALAT1, a competing endogenous RNA of miR-23b-3p, was shown to reduce the suppressive activities of miR-23b-3p on ATG-12, while simultaneously increasing the development of ATG-12, resulting in chemoinduced GC cell autophagy and drug resistance (YiRen et al, 2017). In addition, AKT and mTOR have been reported to be targeted via miR-495 overexpression of miR-495, which could prevent the growth in addition to induce the apoptosis of GC cells through blocking of PI3K/AKT/mTOR, which altered Bax, caspase-3/-9, and cyclin D1 expression (Ouyang et al, 2021). miR-153-3p facilitates ATG-7-mediated autophagy induction in fluorouracil resistance via the adenosine monophosphate (AMP)-activated protein kinase (AMPK)/ATG3 pathway in GC (Hou et al, 2020).…”

Section: Role Of Mirnas Through Regulation Of Autophagy In Gcmentioning

confidence: 99%

“…There are abundant convincing studies that showed inseparable association between miRNAs and GC (Shao et al, 2020). miRNAs affected GC, which includes oncogenesis, diagnosis, development, treatment, and prognosis, although many miRNAs have been linked to GC, and few could be useful to clinical practice (Ouyang et al, 2021), even though numerous miRNAs have been related to GC and few can be applied to clinical practice as well. Furthermore, dietrelated natural ingredients may control autophagy in the GC cell that promote cancer cell chemosensitivity (Xu et al, 2020a).…”

Section: Introductionmentioning

confidence: 99%

Potential Therapeutic Action of Autophagy in Gastric Cancer Managements: Novel Treatment Strategies and Pharmacological Interventions

et al. 2022

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Gastric cancer (GC), second most leading cause of cancer-associated mortality globally, is the cancer of gastrointestinal tract in which malignant cells form in lining of the stomach, resulting in indigestion, pain, and stomach discomfort. Autophagy is an intracellular system in which misfolded, aggregated, and damaged proteins, as well as organelles, are degraded by the lysosomal pathway, and avoiding abnormal accumulation of huge quantities of harmful cellular constituents. However, the exact molecular mechanism of autophagy-mediated GC management has not been clearly elucidated. Here, we emphasized the role of autophagy in the modulation and development of GC transformation in addition to underlying the molecular mechanisms of autophagy-mediated regulation of GC. Accumulating evidences have revealed that targeting autophagy by small molecule activators or inhibitors has become one of the greatest auspicious approaches for GC managements. Particularly, it has been verified that phytochemicals play an important role in treatment as well as prevention of GC. However, use of combination therapies of autophagy modulators in order to overcome the drug resistance through GC treatment will provide novel opportunities to develop promising GC therapeutic approaches. In addition, investigations of the pathophysiological mechanism of GC with potential challenges are urgently needed, as well as limitations of the modulation of autophagy-mediated therapeutic strategies. Therefore, in this review, we would like to deliver an existing standard molecular treatment strategy focusing on the relationship between chemotherapeutic drugs and autophagy, which will help to improve the current treatments of GC patients.

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“…Studies have revealed that RAP2A can 3 Disease Markers regulate cell migration, cytoskeletal recombination, and other cellular processes [5][6][7]. In addition, it has been reported that RAP2A is upregulated in prostate cancer, thyroid cancer, nasopharyngeal cancer, and other human cancers [8][9][10]. However, the expression of RAP2A in GC has not been reported, except for one study that detected high expression of Rap2A in human hepatoblastoma HepG2 cells.…”

Section: Introductionmentioning

confidence: 99%

miR-33a-5p Targets RAP2A to Mediate the Sensitivity of Gastric Cancer Cells to 5-FU

et al. 2022

Disease Markers

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Objective. The objective of this study is to explore the effects of microRNA-33a-5p (miR-33a-5p)-ras-related protein Rap-2a (RAP2A) on biological functions of gastric cancer (GC) and to find the potential functional mechanism. Methods. We measured the miR-33a-5p expression in 30 GC tissues and cellular level and 30 adjacent normal tissues as control. Besides, the expression of miR-33a-5p was checked at cell level as well. To screen the possible targets of miR-33a-5p, prediction software was used and gene RAP2A attracted our attention. Through a series of experiments including real-time polymerase chain reaction (qRT-PCR), luciferase assay, and western blotting (WB), we verified RAP2A as a potential target of miR-33a-5p. The impacts of miR-33a-5p and RAP2A on biological functions of GC cell lines (BGC-823 and MGC-803) were analyzed by subsequent experiments. Cell invasion was tested by invasion assays. Cell proliferation was measured by cell counting kit-8 (CCK-8) assay. Cell clone was measured by clone formation assays. Finally, the expression of RAP2A protein was analyzed by WB assay. Results. We found miR-33a-5p was expressed lowly in GC tissues and cells. Overexpression of miR-33a-5p in BGC-823 and MGC-803 cells greatly inhibited the cell invasion and colony number. Furthermore, compared to sh-control (shControl), RAP2A knockdown (sh-RAP2A/shRAP2A) raised the sensitivity of GC cells to 5-FU significantly, characterized as reducing cell apoptosis. Conclusions. The expression of miR-33a-5p was lower in GC cell lines and tissues obviously, indicating that miR-33a-5p served as the antitumor gene in GC. The expression of RAP2A regulated negatively the sensitivity of GC cells to 5-FU. According to our in vitro experiments, miR-33a-5p/RAP2A was likely to become a new therapeutic target for GC.

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Clinical crosstalk between microRNAs and gastric cancer (Review)

Cited by 21 publications

References 136 publications

Aberrant expression of SFRP1, SFRP3, DVL2 and DVL3 Wnt signaling pathway components in diffuse gastric carcinoma

Aberrant expression of SFRP1, SFRP3, DVL2 and DVL3 Wnt signaling pathway components in diffuse gastric carcinoma

Potential Therapeutic Action of Autophagy in Gastric Cancer Managements: Novel Treatment Strategies and Pharmacological Interventions

miR-33a-5p Targets RAP2A to Mediate the Sensitivity of Gastric Cancer Cells to 5-FU

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