Induction of miR-31 causes increased sensitivity to 5-FU and decreased migration and cell invasion in gastric adenocarcinoma

Korourian, Alireza; Madjd, Zahra; Roudi, Raheleh; Shariftabrizi, Ahmad; Soleimani, M

doi:10.4149/bll_2019_005

Cited by 17 publications

(15 citation statements)

References 25 publications

(42 reference statements)

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“…23 Korourian et al indicated that the upregulation of miR-31 could increase the sensitivity of gastric cancer cells to 5-Fu in gastric adenocarcinoma. 24 Qin et al found that miR-106a could decrease the sensitivity of colorectal cancer cells to 5-Fu. 25 In the present study, we found that knockdown of miR-486-5p enhanced the inhibitory effects of 5-Fu on the migration and invasion of PANC-1 cells.…”

Section: Discussionmentioning

confidence: 99%

Downregulation of miR-486-5p Enhances the Anti-Tumor Effect of 5-Fluorouracil on Pancreatic Cancer Cells

Wang

Liu

Sun

et al. 2020

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These authors contributed equally to this work Background: 5-Fluorouracil (5-Fu) has been applied to treat pancreatic cancer, which is one of the most common types of digestive system tumors. Evidence has shown that miR-486-5p could promote the proliferation of pancreatic cancer cells. Therefore, this study aimed to investigate whether downregulation of miR-486-5p could enhance the anti-tumor effect of 5-Fu on pancreatic cancer cells. Methods: Cell Counting Kit 8 assay, flow cytometry and wound healing assays were used to detect proliferation, apoptosis and migration in PANC-1 cells. The expressions of Bcl-2, Bax, cleaved caspase 3, PTEN, p-Akt and p-ERK in PANC-1 cells were detected with Western blot assay. Results: In this study, the inhibitory effects of 5-Fu on the proliferation, migration and invasion of PANC-1 cells were significantly enhanced following transfection with miR-486-5p antagonist. In addition, downregulation of miR-486-5p markedly enhanced the proapoptosis effect of 5-Fu on PANC-1 cells. Moreover, bioinformatics analysis and luciferase reporter assay identified that PTEN was the directly binding target of miR-486-5p. Meanwhile, downregulation of miR-486-5p markedly enhanced the anti-tumor effect of 5-Fu in PANC-1 cells via upregulation of the level of PTEN, and downregulation of the expressions of p-ERK and p-Akt. In vivo experiments confirmed that knockdown of miR-486-5p could enhance the anti-tumor effect of 5-Fu in PANC-1 xenograft model. Conclusion: We found that the downregulation of miR-486-5p could enhance the antitumor effect of 5-Fu on pancreatic cancer cells. Therefore, miR-486-5p antagonist plus 5-Fu might be considered as a potential therapeutic strategy for the treatment of pancreatic cancer.

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Section: Discussionmentioning

confidence: 99%

Downregulation of miR-486-5p Enhances the Anti-Tumor Effect of 5-Fluorouracil on Pancreatic Cancer Cells

Wang

Liu

Sun

et al. 2020

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“…MicroRNAs (miRNAs) belong to a class of small noncoding RNAs that are involved in development and diseases, making miRNAs an attractive tool and target for novel therapeutic approaches . Many miRNAs such as miR‐31 have been reported to be closely related to the development of GC, including the migration, metastasis, and the sensitivity to anticancer drugs of GC . miRNAs have also been reported to be associated with the initiation of chief cell transdifferentiation and apoptosis .…”

Section: Introductionmentioning

confidence: 99%

miR‐133a‐3p/FOXP3 axis regulates cell proliferation and autophagy in gastric cancer

Zhang

Liu

et al. 2020

J of Cellular Biochemistry

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Although many methods and new therapeutic drugs have been developed, the overall survival rate and long-term survival rate of patients with gastric cancer (GC) are still not satisfactory. In this study, we investigated the effects of microRNA miR-133a-3p and transcription factor FOXP3 on proliferation and autophagy of GC cells and their interactions. Our results showed that knockdown of FOXP3 increased the proliferation and autophagy of GC cells.The relationship between FOXP3 and autophagy has not been reported previously. In addition, FOXP3 could directly bind the promoter region of TP53 and inhibit its expression. miR-133a-3p increased the proliferation and autophagy via decreasing the protein level of FOXP3 by targeting its 3′-UTR. Our research provides new insights into the development of GC and provides new ideas and theoretical basis for the clinical treatment of GC and the development of new drug targets. K E Y W O R D S autophagy, FOXP3, gastric cancer, miR-133a-3p, proliferation

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“…For example, overexpression of miR-939, miR-623, miR-429, miR-204, miR-124 or miR-31 was shown to enhance 5-FUinduced chemosensitivity by compromising tumor cell growth or inducing apoptosis. 9,[13][14][15][16][17][18][19] Among the above-mentioned miRNAs, miR-939 and miR-204 were the only two miRNAs with confirmed ability of reversing drug resistance both in vitro and in vivo, providing more convening evidence than others. 9,15 A role of miR-31 in chemosensitivity was reported by two separate research groups and may have more obvious effects.…”

Section: Microrna-based Chemotherapy Fluorouracil Resistancementioning

confidence: 99%

“…9,15 A role of miR-31 in chemosensitivity was reported by two separate research groups and may have more obvious effects. [17][18][19] Moreover, reduced miR-6785-5p, miR-193-3p, or miR-147 expression could also increase the chemosensitivity of GC to 5-FU. [20][21][22] Interestingly, miR-193-3p and miR-147 both target phosphatase and tensin homolog (PTEN) to exert their functions in GC.…”

Section: Microrna-based Chemotherapy Fluorouracil Resistancementioning

confidence: 99%

Research Progress in microRNA-Based Therapy for Gastric Cancer

Zhao

Shi

et al. 2019

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Gastric cancer (GC) is one of the leading causes of tumor-related mortality. In addition to surgery and endoscopic resection, systemic therapy remains the main treatment option for GC, especially for advanced-stage disease and for cases not suitable for surgical therapy. Hence, improving the efficacy of systemic therapy is still an urgent problem to overcome. In the past decade, the essential roles of microRNAs (miRNAs) in tumor treatment have been increasingly recognized. In particular, miRNAs were recently shown to reverse the resistance to chemotherapy drugs such as 5-fluorouracil, cisplatin, and doxorubicin. Synthesized nanoparticles loaded with mimics or inhibitors of miRNAs can directly target tumor cells to suppress their growth. Moreover, exosomes may serve as promising safe carriers for mimics or inhibitors of miRNAs to treat GC. Some miRNAs have also been shown to play roles in the mechanism of action of other anti-tumor drugs. Therefore, in this review, we highlight the research progress on microRNA-based therapy in GC and discuss the challenges and prospects associated with this strategy. We believe that microRNA-based therapy has the potential to offer a clinical benefit to GC patients, and this review would contribute to and motivate further research to promote this field toward this ultimate goal.

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Induction of miR-31 causes increased sensitivity to 5-FU and decreased migration and cell invasion in gastric adenocarcinoma

Cited by 17 publications

References 25 publications

<p>Downregulation of miR-486-5p Enhances the Anti-Tumor Effect of 5-Fluorouracil on Pancreatic Cancer Cells</p>

<p>Downregulation of miR-486-5p Enhances the Anti-Tumor Effect of 5-Fluorouracil on Pancreatic Cancer Cells</p>

miR‐133a‐3p/FOXP3 axis regulates cell proliferation and autophagy in gastric cancer

<p>Research Progress in microRNA-Based Therapy for Gastric Cancer</p>

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