miRNA-135a promotes hepatocellular carcinoma cell migration and invasion by targeting forkhead box O1

Zeng, Yue-bin; Liang, Xing-Hua; Zhang, Guang‐Xian; Jiang, Nan; Zhang, Tong; Huang, Jianying; Zhang, Lei; Zhang, Xiancheng

doi:10.1186/s12935-016-0328-z

Cited by 72 publications

(49 citation statements)

References 24 publications

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“…High miR-135a levels favour invasive and metastatic growth of HCC cells in vitro and are correlated with malignant portal vein thrombosis, possibly by directly targeting MTSS1 [20]. Other targets of miR-135a investigated in vitro are forkhead box O1, matrix metalloproteinase-2, AKT pathway, and Krüppel-like factor-4 [21, 22]. Therefore, from a functional perspective, elevated levels of miR-135a might induce early formation of microscopic HCC dissemination via several pathways, and thus, result in early HCC recurrence after curative resection.…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, Liu et al showed that overexpression of miR-135a favours an invasive and metastatic behaviour of HCC in vitro and is associated with malignant portal vein thrombosis in vivo, most likely by directly targeting metastasis suppressor 1 (MTSS1) [20]. Two other studies showed that miR-135a also down-regulates Krüppel-like factor 4, up-regulates the expression of matrix metalloproteinase-2 and Akt, and down-regulates forkhead box O1, resulting in higher proliferation and invasiveness of HCC cells [21, 22]. …”

Section: Introductionmentioning

confidence: 99%

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High expression of micro RNA-135A in hepatocellular carcinoma is associated with recurrence within 12 months after resection

et al. 2017

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BackgroundHepatocellular carcinoma has a dismal prognosis due to recurrence rates of up to 70% after curative resection. Early recurrence is driven by synchronous microscopic intrahepatic metastases. The predictive value of histological parameters is discussed controversially and adjuvant therapy is not established. The aim of this study was to identify patients at high risk for early intrahepatic recurrence by expression profiling of selected micro RNAs.MethodsIn 52 patients undergoing HCC resection between 2011 and 2014, liver and tumor tissue was collected during surgery. Twelve patients with incomplete data regarding HCC recurrence, secondary liver transplantation, or perioperative death were excluded, leaving 40 patients with early recurrence <12 months (R+) or without recurrence for >24 months (R-) to compare grading, T, L, V, and R status. If tissue quality permitted, micro RNAs were measured in HCC and liver tissue.ResultsTen women and 30 men (64.0 ± 10.2 years) were analyzed. R+ occurred in 29 patients 6.2 ± 4.5 months after resection. Surveillance of R- was 26.2 ± 5.2 months. High intratumoral expression of miR-135a was associated with high risk of recurrence (HR = 4.2, p = 0.024, time to recurrence 8.8 ± 2.0 vs. 24.8 ± 4.4 months in patients with low miR-135a expression). As expected, T3 status was correlated with early recurrence, while other histological parameters and expression of miR-21, miR-122, and miR-125a did not.ConclusionsWe show a significant association between high expression of miR-135a and early HCC recurrence. Therefore, high intratumoral miR-135a expression might serve as a novel biomarker to identify patients urgently requiring adjuvant therapy post resection.Electronic supplementary materialThe online version of this article (doi:10.1186/s12885-017-3053-7) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

High expression of micro RNA-135A in hepatocellular carcinoma is associated with recurrence within 12 months after resection

et al. 2017

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“…MiR-135a reportedly enhances cellular proliferation in multiple malignancies, including colorectal cancer [33], hepatocellular carcinoma [34], and melanoma [35]. It also purportedly promotes tumour formation in bladder cancer and suppresses p21 expression [26].…”

Section: Discussionmentioning

confidence: 99%

CircRNA-Cdr1as Exerts Anti-Oncogenic Functions in Bladder Cancer by Sponging MicroRNA-135a

Yang

Yuan

et al. 2018

Cell Physiol Biochem

129

108

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Background/Aims: CircRNAs regulate gene expression in different malignancies. However, the role of Cdr1as in the tumourigenesis of bladder cancer and its potential mechanisms remain unknown. Methods: qRT-PCR was used to detect Cdr1as and target miRNA expression in bladder cancer tissues and cell lines. Biological functional experiments were performed to detect the effects of Cdr1as on the biological behaviour of bladder cancer cells in vivo and in vitro. Bioinformatic analysis was utilised to predict potential miRNA target sites on Cdr1as. Ago2 RNA binding protein immunoprecipitation assay, RNA antisense purification assay, biotin pull down assay and RNA FISH were performed to detect the interaction between Cdr1as and target miRNAs. Western blot was used to determine the expression level of p21 in bladder cancer cells. Results: Cdr1as was significantly down-regulated in bladder cancer tissues compared with adjacent normal tissues. Overexpression of Cdr1as inhibited the proliferation, invasion and migration of bladder cancer cells in vitro and slowed down tumour growth in vivo. Cdr1as sponged multiple miRNAs in bladder cancer. Moreover, Cdr1as directly bound to miR-135a and inhibited its activity in bladder cancer. Conclusion: Cdr1as is down-regulated and sponges multiple miRNAs in bladder cancer. It exerts anti-oncogenic functions by sponging microRNA-135a.

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“…Likewise, cell proliferation is suppressed in HCC due to let-7a and let-7 g that regulates the oncogenic STAT3 and cMyc, respectively [42]. miRNA-135a targets fork-head box O1 and miRNA-155-3p suppresses FBXW7 leading to an increased invasion and migration in HCC [56, 153]. miRNA-186 targets Yes-associated protein 1 and acts as a potential therapeutic target in treating HCC [48].…”

Section: Noncoding Rnasmentioning

confidence: 99%

New Insights into the Epigenetics of Hepatocellular Carcinoma

Wahid

Ali

Rafique

et al. 2017

BioMed Research International

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Hepatocellular Carcinoma (HCC) is one of the most predominant malignancies with high fatality rate. This deadly cancer is rising at an alarming rate because it is quite resistant to radio- and chemotherapy. Different epigenetic mechanisms such as histone modifications, DNA methylation, chromatin remodeling, and expression of noncoding RNAs drive the cell proliferation, invasion, metastasis, initiation, progression, and development of HCC. These epigenetic alterations because of potential reversibility open way towards the development of biomarkers and therapeutics. The contribution of these epigenetic changes to HCC development has not been thoroughly explored yet. Further research on HCC epigenetics is necessary to better understand novel molecular-targeted HCC treatment and prevention. This review highlights latest research progress and current updates regarding epigenetics of HCC, biomarker discovery, and future preventive and therapeutic strategies to combat the increasing risk of HCC.

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miRNA-135a promotes hepatocellular carcinoma cell migration and invasion by targeting forkhead box O1

Cited by 72 publications

References 24 publications

High expression of micro RNA-135A in hepatocellular carcinoma is associated with recurrence within 12 months after resection

High expression of micro RNA-135A in hepatocellular carcinoma is associated with recurrence within 12 months after resection

CircRNA-Cdr1as Exerts Anti-Oncogenic Functions in Bladder Cancer by Sponging MicroRNA-135a

New Insights into the Epigenetics of Hepatocellular Carcinoma

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