miR-203 Acts as a Tumor Suppressor Gene in Osteosarcoma by Regulating RAB22A

Yang, Dongfang; Liu, Guang Peng; Wang, Kunzheng

doi:10.1371/journal.pone.0132225

Cited by 45 publications

(30 citation statements)

References 46 publications

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“…These findings suggest that the upregulation of RAB22A in melanoma may partly be due to the decreased expression of miR-203. In fact, the targeting relationship between miR-203 and RAB22A was also reported in osteosarcoma [13]. Therefore, our study expands the importance of miR-203/RAB22A axis in human cancers.…”

Section: Discussionsupporting

confidence: 75%

RAB22A overexpression promotes the tumor growth of melanoma

Chen

Zhu

et al. 2016

Oncotarget

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Malignant melanoma is the most aggressive type of skin cancer. RAB22A, a member of RAS oncogene family, has been found to be significantly upregulated in multiple human cancers. In the present study, we found that RAB22A mRNA expression was significantly upregulated in melanoma tissues (including 60 primary melanomas and 84 metastatic melanomas) compared to benign nevi (n = 20), which were significantly higher in metastatic melanoma tissues than primary tissues. Immunohistochemistry data further showed that the positive immunoreactivity of RAB22A was detected in 66% (95/144) melanoma tissues, but not in benign nevi. Moreover, high expression of RAB22A was significantly associated with advanced clinical stage in melanoma. Furthermore, patients with high RAB22A expression had shorter overall survival compared those with low expression of RAB22A. In-vitro study showed that RAB22A was also upregulated in melanoma cell lines WM35, A375, WM451, and SK-MEL-1, when compared with the normal melanocyte HM cells. Knockdown of RAB22A significantly reduced the proliferation, migration and invasion of melanoma A375 cells, while overexpression of RAB22A significantly promoted these malignant phenotypes. In addition, RAB22A was found to be a target of miR-203, a tumor suppressive miRNA in melanoma. Besides, miR-203 was downregulated in melanoma tissues and cell lines, when compared with benign nevi and HM cells, respectively. Taken these findings together, our study could validate an oncogenic role of RAB22A in melanoma, suggesting that RAB22A may be a potential therapeutic target for melanoma.

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Section: Discussionsupporting

confidence: 75%

RAB22A overexpression promotes the tumor growth of melanoma

Chen

Zhu

et al. 2016

Oncotarget

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“…Zhang et al found that miR-373 targeting of the Rab22a oncogene suppressed tumor invasion and metastasis in ovarian cancer (30). miR-203 has been reported as a tumor-suppressor gene in osteosarcoma by regulating RAB22A (31). The present study identified that miR-204 inhibited RAB22A expression by directly targeting 3'UTR of RAB22A in RCC.…”

Section: Discussionsupporting

confidence: 56%

miR-204 inhibits the proliferation and invasion of renal cell carcinoma by inhibiting RAB22A expression

et al. 2016

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Abstract. While miR-204 expression may be linked to renal cell carcinoma (RCC) progression, the detailed mechanisms remain unclear. In the present study, we demonstrated that miR-204 was differentially expressed in RCC tissues when compared with surrounding normal kidney tissues. Ectopic overexpression of miR-204 in human RCC cells suppressed cell proliferation and invasion in vitro and in vivo. Mechanism dissection revealed that miR-204 may function through RAB22A signals to inhibit RCC proliferation and invasion. Overexpression of RAB22A by oe-RAB22A was able to partially reverse the miR-204-mediated suppression of RCC tumor progression. Together, these results revealed that miR-204 suppressed RCC proliferation and invasion by directly targeting the RAB22A gene. Targeting newly identified RAB22A with miR-204 may aid in the suppression of RCC proliferation and invasion.

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“…miR-203 also plays important roles in cancerigenesis. miR-203 has been reported to be the tumor suppressor in osteosarcoma (29). miR-203 also directly targeted oncogene ADAM9 and long non-coding RNA HULC to inhibit the hepatocellular carcinoma cell proliferation and metastasis (30).…”

Section: Discussionmentioning

confidence: 99%

Sevoflurane suppresses proliferation by upregulating microRNA-203 in breast cancer cells

et al. 2018

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Rapid proliferation is one of the critical characteristics of breast cancer. However, the underlying regulatory mechanism of breast cancer cell proliferation is largely unclear. The present study indicated that sevoflurane, one of inhalational anesthetics, could significantly suppress breast cancer cell proliferation by arresting cell cycle at G1 phase. Notably, the rescue experiment indicated that miR-203 was upregulated by sevoflurane and mediated the function of sevoflurane on suppressing the breast cancer cell proliferation. The present study indicated the function of the sevoflurane/miR-203 signaling pathway on regulating breast cancer cell proliferation. These results provide mechanistic insight into how the sevoflurane/miR-203 signaling pathway supresses proliferation of breast cancer cells, suggesting the sevoflurane/miR-203 pathway may be a potential target in the treatment of breast cancer.

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miR-203 Acts as a Tumor Suppressor Gene in Osteosarcoma by Regulating RAB22A

Cited by 45 publications

References 46 publications

RAB22A overexpression promotes the tumor growth of melanoma

RAB22A overexpression promotes the tumor growth of melanoma

miR-204 inhibits the proliferation and invasion of renal cell carcinoma by inhibiting RAB22A expression

Sevoflurane suppresses proliferation by upregulating microRNA-203 in breast cancer cells

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