Tumor suppressor miR-24 restrains gastric cancer progression by downregulating RegIV

Duan, Yongrui; Hu, Lei; Liu, Bing; Yu, Beiqin; Li, Jianfang; Yan, Min; Yu, Yingyan; Li, Chen; Su, Liping; Zhu, Zhenggang; Xiang, Ming; Liu, Bing-ya; Yang, Qun

doi:10.1186/1476-4598-13-127

Cited by 63 publications

(61 citation statements)

References 41 publications

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“…miRNAs are important regulators in the development of gastric adenocarcinoma (Duan et al, ; Kang et al, ; Shen et al, ). miR‐665 is a newly identified miRNA in cancers.…”

Section: Discussionmentioning

confidence: 99%

miR‐665 promotes the progression of gastric adenocarcinoma via elevating FAK activation through targeting SOCS3 and is negatively regulated by lncRNA MEG3

Tang

Long

Zhuang

et al. 2019

Journal Cellular Physiology

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Studies have found that miR-665 acted as a tumor suppressor or an oncogene in different malignancies. miR-665 expression was elevated in gastric adenocarcinoma tissues; however, its role and mechanism in this disease are not fully clarified. The expression of miR-665 and its target gene was detected in human gastric adenocarcinoma tissues and cells. Moreover, we analyzed the effects of miR-665 on the proliferation, migration, and epithelial-mesenchymal transition (EMT) of gastric adenocarcinoma cells as well as tumor growth in vivo. The mechanisms of miR-665 in gastric adenocarcinoma were investigated by using molecular biology techniques. We found miR-665 was upregulated and suppressor of cytokine signaling 3 (SOCS3) was downregulated in gastric adenocarcinoma tissues and cells. Elevated miR-665 was positively correlated with tumor size, lymph node metastasis, invasion depth, TNM stage, and poor differentiation in gastric adenocarcinoma patients. Overexpression of miR-665 promoted, whereas knockdown of miR-665 suppressed the proliferation, migration, and EMT of gastric adenocarcinoma cells. Furthermore, we demonstrated that miR-665 functioned through targeting SOCS3, followed by activation of the FAK/ Src signaling pathway in gastric adenocarcinoma cells. miR-665 antagomir inhibited tumor growth as well as the activation of the FAK/Src pathway but increased SOCS3 expression in nude mice. In addition, miR-665 expression was negatively regulated by long noncoding RNA maternally expressed gene 3 (MEG3). In conclusion, miR-665 acted as an oncogene in gastric adenocarcinoma by inhibiting SOCS3 followed by activation of the FAK/Src pathway and it was negatively modulated by MEG3. miR-665 may be a promising therapeutic target for the treatment of gastric adenocarcinoma. K E Y W O R D SFAK/Src pathway, gastric adenocarcinoma, lncRNA MEG3, miR-665, SOCS3

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“…miRNAs are important regulators in the development of gastric adenocarcinoma (Duan et al, ; Kang et al, ; Shen et al, ). miR‐665 is a newly identified miRNA in cancers.…”

Section: Discussionmentioning

confidence: 99%

miR‐665 promotes the progression of gastric adenocarcinoma via elevating FAK activation through targeting SOCS3 and is negatively regulated by lncRNA MEG3

Tang

Long

Zhuang

et al. 2019

Journal Cellular Physiology

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“…In addition, miR-24 could promote cell proliferation in lung cancer (25) and hepatocellular carcinoma (26). However, miR-24 could inhibit cell proliferation in gastric cancer (27,28), and acts as a tumor suppressor in colon cancer (29). In breast cancer, the role of miR-24 also remains controversial.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of microRNA-24 increases the sensitivity to paclitaxel in drug-resistant breast carcinoma cell lines via targeting ABCB9

et al. 2016

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Paclitaxel has been widely used in the treatment of breast cancer. However, the development of drug resistance often increases the failure of chemotherapy. Growing evidence has reported the significant role of microRNAs (miRs) in drug resistance. The present study identified that miR-24 was significantly downregulated in paclitaxel-resistant (PR) breast cancer patients and in MCF-7/PR human breast carcinoma cells, and that overexpression of miR-24 could increase the effect of paclitaxel on drug-resistant breast carcinoma cells. Furthermore, miR-24 could directly bind to the 3′-untranslated region of ATP binding cassette B9 to downregulate its expression, thereby reducing drug transportation and improving the anti-tumor effect of paclitaxel on breast cancer cells. In vivo experiments also demonstrated that overexpression of miR-24 could increase the sensitivity of drug-resistant MCF-7 cells to paclitaxel. In conclusion, the present results suggested a novel function for miR-24 in reducing paclitaxel resistance in breast cancer, which may be of important clinical significance.

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“…A previous study [17] showed that miR-24 is downregulated in GC tissues compared with matched nontumor tissues and that ectopic expression of miR-24 in GC cells suppressed cell proliferation, migration, and invasion in vitro as well as tumorigenicity in vivo. Furthermore, upregulation of miR-24 in terminally differentiated cells has been demonstrated [18].…”

Section: Discussionmentioning

confidence: 99%

“…Ectopic expression of miR-24 in GC cells suppressed cell proliferation, migration, and invasion in vitro as well as tumorigenicity in vivo [17]. The mechanisms of downregulation of miR-24 in GC have not yet been completely investigated.…”

Section: Discussionmentioning

confidence: 99%

Characteristic <b><i>miR-24</i></b> Expression in Gastric Cancers among Atomic Bomb Survivors

et al. 2015

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Objective: To elucidate the mechanism of radiation-induced cancers, we analyzed the expression profiles of microRNAs extracted from formalin-fixed paraffin-embedded (FFPE) gastric cancer (GC) tissue samples from atomic bomb survivors. Methods: The expression levels of miR-21, miR-24, miR-34a, miR-106a, miR-143, and miR-145 were measured by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Results: The expression of microRNAs was measured by qRT-PCR in a Hiroshima University Hospital cohort comprising 32 patients in the high-dose-exposed group and 18 patients in the low-dose-exposed group who developed GC after the bombing. The GC cases showing high expression of miR-24, miR-143, and miR-145 were more frequently found in the high-dose-exposed group than in the low-dose-exposed group. We next performed qRT-PCR of miR-24, miR-143, and miR-145 in a cohort from the Hiroshima Red Cross Hospital and Atomic-Bomb Survivors Hospital comprising 122 patients in the high-dose-exposed group and 48 patients in the low-dose-exposed group who developed GC after the bombing. High expressions of miR-24 and miR-143 were more frequently found in the high-dose-exposed group than in the low-dose-exposed group. Multivariate analysis demonstrated that only high expression of miR-24 was an independent predictor for the exposure status. Conclusion: These results suggest that the measurement of miR-24 expression from FFPE samples is useful to identify radiation-associated GC.

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Tumor suppressor miR-24 restrains gastric cancer progression by downregulating RegIV

Cited by 63 publications

References 41 publications

miR‐665 promotes the progression of gastric adenocarcinoma via elevating FAK activation through targeting SOCS3 and is negatively regulated by lncRNA MEG3

miR‐665 promotes the progression of gastric adenocarcinoma via elevating FAK activation through targeting SOCS3 and is negatively regulated by lncRNA MEG3

Overexpression of microRNA-24 increases the sensitivity to paclitaxel in drug-resistant breast carcinoma cell lines via targeting ABCB9

Characteristic <b><i>miR-24</i></b> Expression in Gastric Cancers among Atomic Bomb Survivors

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