MicroRNA-203 induces apoptosis by upregulating Puma expression in colon and lung cancer cells

Funamizu, Naotake; Lacy, Curtis; Kamada, Minori; Yanaga, Katsuhiko; Manome, Yoshinobu

doi:10.3892/ijo.2015.3178

Cited by 21 publications

(11 citation statements)

References 45 publications

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“…In the present study, we found that expression of miR‐203 significantly suppressed NSCLC cell growth, and decreased cell migration and invasion as reported in previous studies . However, overexpression of RGS17 reversed the miR‐203‐induced antitumor effect.…”

Section: Discussionsupporting

confidence: 90%

“…In the present study, we found that expression of miR-203 significantly suppressed NSCLC cell growth, and decreased cell migration and invasion as reported in previous studies. (18,19,24,28,29) However, overexpression of RGS17 reversed the miR-203-induced antitumor effect. The bifluorescein test further verified that miR-203 integrated into the 3 0 -UTR of RGS-17 and post-transcriptionally downregulated RGS-17 expression.…”

Section: Discussionmentioning

confidence: 98%

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miR‐203 inhibits cell proliferation, invasion, and migration of non‐small‐cell lung cancer by downregulating RGS17

et al. 2017

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Involvement of the RGS17 oncogene in the promotion of non‐small‐cell lung cancer (NSCLC) has been reported, but the regulation mechanism in NSCLC remains unclear. MicroRNAs (miRNAs) negatively regulate gene expression, and their dysregulation has been implicated in tumorigenesis. To understand the role of miRNAs in Regulator of G Protein Signaling 17 (RGS17)‐induced NSCLC, we showed that miR‐203 was downregulated during tumorigenesis, and inhibited the proliferation and invasion of lung cancer cells. We then determined whether miR‐203 regulated NSCLC by targeting RGS17. To characterize the regulatory effect of miR‐203 on RGS17, we used lung cancer cell lines, A549 and Calu‐1, and the constructed miR‐203 and RGS17 overexpression vectors. The CCK8 kit was used to determine cell proliferation, and the Transwell® assay was used to measure cell invasion and migration. RT‐PCR, western blots, and immunofluorescence were used to analyze expression of miR‐203 and RGS17, and the luciferase reporter assay was used to examine the interaction between miR‐203 and RGS17. Nude mice were used to characterize in vivo tumor growth regulation. Expression of miR‐203 inhibited proliferation, invasion, and migration of lung cancer cell lines A549 and Calu‐1 by targeting RGS17. The regulatory effect of miR‐203 was inhibited after overexpression of RGS17. The luciferase reporter assay showed that miR‐203 downregulated RGS17 by direct integration into the 3′‐UTR of RGS17 mRNA. In vivo studies showed that expression of miR‐203 significantly inhibited growth of tumors. Taken together, the results suggested that expression of miR‐203 inhibited tumor growth and metastasis by targeting RGS17.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 98%

miR‐203 inhibits cell proliferation, invasion, and migration of non‐small‐cell lung cancer by downregulating RGS17

et al. 2017

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“…PUMA also functioned through other Bcl-2 family members, such as Bcl-2, Bcl-XL and Bax (32). Although the specific mechanism for PUMA inducing apoptosis needs further investigation, it has been shown to be a promising new terget in gene therapy (33,34). The goal of this study was to explore the effect of combining Slug siRNA with X-ray irradiation on HSC3 and HSC6 cells.…”

Section: Discussionmentioning

confidence: 99%

Slug inhibition increases radiosensitivity of oral squamous cell carcinoma cells by upregulating PUMA

Jiang

Zhou

Wei

et al. 2016

International Journal of Oncology

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As a new strategy, radio-gene therapy was widely used for the treatment of cancer patients in recent few years. Slug was involved in the radioresistance of various cancers and has been found to have an anti-apoptotic effect. This study aims to investigate whether the modulation of Slug expression by siRNA affects oral squamous cell carcinoma sensitivity to X-ray irradiation through upregulating PUMA. Two oral squamous cell carcinoma cell lines (HSC3 and HSC6) were transfected with small interfering RNA (siRNA) targeting Slug and subjected to radiotherapy in vitro. After transfection with Slug siRNA, both HSC3 and HSC6 cells showed relatively lower expression of Slug and higher expression of PUMA. The Slug siRNA transfected cells showed decreased survival and proliferation rates, an increased apoptosis rate and enhanced radiosensitivity to X-ray irradiation. Our results revealed that Slug siRNA transfection in combination with radiation increased the expression of PUMA, which contributed to radiosensitivity of oral squamous cell carcinoma cells. Thus, controlling the expression of Slug might contribute to enhance sensitivity of HSC3 and HSC6 cells toward X-ray irradiation in vitro by upregulating PUMA.

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“…25,39 Moreover, miR-203 controls cell proliferation in haematopoietic malignancies by targeting ABL1 23 and induces apoptosis in colon and lung cancer cells by upregulating the expression of Puma. 40 However, the functions of miR-203 in Xinjiang Kazak ESCC remain unambiguous and warrant further studies.…”

Section: Discussionmentioning

confidence: 97%

Epigenetic silencing of miR-203 in Kazakh patients with esophageal squamous cell carcinoma by MassARRAY spectrometry

et al. 2017

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Dysregulation of miR-203 by promoter methylation is associated with the development of various cancers. We aimed to explore the underlying link between promoter methylation and miR-203 expression in Kazakh esophageal squamous cell carcinoma (ESCC). MassARRAY® System spectrometry was used to quantitatively analyze the DNA methylation of 32 CpG sites within miR-203 in 99 Kazakh ESCC and 46 normal esophageal tissues (NETs) with similar population characteristics. We conducted real-time PCR to detect miR-203 expression levels and evaluated their association with methylation. Eleven CpG units within miR-203 promoter were frequently hypermethylated in ESCC compared with NETs (P < 0.05). The hypermethylation of several CpG units positively correlated with age, lower esophagus, constrictive type of ESCC, and moderately differentiated ESCC. Given the involvement of human papillomavirus (HPV) in etiology of ESCC was confirmed from our previous reports, herein we found that CpG units within miR-203 in HPV16-positive ESCC are more heavily methylated. Furthermore, miR-203 expression showed a nearly 4.5-fold decrease in ESCC than NETs (0.206 ± 0.336 vs. 0.908 ± 1.424, P < 0.001) and was significantly associated with lymph node metastasis (P = 0.012). The expression of miR-203 with 11 completely hypermethylated CpG units was approximately 6.5-fold lower than that with at least 1 unmethylated CpG unit (P < 0.001) and especially the CpG_15.16 and CpG_31.32 with higher methylation levels in ESCC tissues exhibited lower expression levels of miR-203, which indicated a reverse association between miR-203 methylation and expression. Hypermethylated miR-203 is a potential biomarker and targeted delivery of miR-203 could therefore serve as a preventive or therapeutic strategy for Kazakh ESCC.

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MicroRNA-203 induces apoptosis by upregulating Puma expression in colon and lung cancer cells

Cited by 21 publications

References 45 publications

miR‐203 inhibits cell proliferation, invasion, and migration of non‐small‐cell lung cancer by downregulating RGS17

miR‐203 inhibits cell proliferation, invasion, and migration of non‐small‐cell lung cancer by downregulating RGS17

Slug inhibition increases radiosensitivity of oral squamous cell carcinoma cells by upregulating PUMA

Epigenetic silencing of miR-203 in Kazakh patients with esophageal squamous cell carcinoma by MassARRAY spectrometry

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