MiR-124 suppresses tumor growth and metastasis by targeting Foxq1 in nasopharyngeal carcinoma

Peng, Xiao Hong; Huang, Hao; Lü, Juan; Liu, Xiong; Zhao, Fei; Bao, Zhenan; Lin, Shao Xiong; Wang, Lu; Chen, Huai Hong; Xu, Xia; Wang, Fan; Li, Xiang Ping

doi:10.1186/1476-4598-13-186

Cited by 103 publications

(110 citation statements)

References 40 publications

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“…miR-124 suppressed tumor growth and metastasis by targeting FOXQ1 in nasopharyngeal cancer (50). An additional previous study suggested that there was a double-negative feedback loop between miR-422a and its targeted gene, FOXQ1, in HCC (51).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑1271 inhibits cellular proliferation of hepatocellular carcinoma

et al. 2017

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Abstract. Hepatocellular carcinoma (HCC) is one of the most common causes of cancer-associated mortality worldwide, particularly in China. MicroRNAs (miRs) serve important roles in the pathogenesis of HCC. The present study investigated the function of miR-1271 in HCC. The miR-1271 levels were analyzed by quantitative reverse transcription polymerase chain reaction. Cells growth was examined by MTT assay. Bioinformatics algorithms from TargetScanHuman were used to predict the target genes of miR-1271. The protein level was assayed by western blotting. miR-1271 demonstrated a lower expression level in HCC tissues. Upregulation of miR-1271 suppressed the growth of HepG-2 and Huh-7 cells and induced apoptosis of cells. Forkhead box Q1 (FOXQ1) was targeted by miR-1271. In conclusion, miR-1271 is a novel tumor suppressor that inhibits HCC proliferation and induces cellular apoptosis by targeting FOXQ1 in HCC. The results of the present study may provide a novel therapeutic target of HCC. IntroductionHepatocellular carcinoma (HCC) accounts for ~80% of all liver cancer cases, and is one of the most common causes of cancer-associated mortality worldwide (1,2). The prevalence rate of HCC in China is particularly high, but continues to increase in numerous western countries (1,3). Despite HCC being was one of the first cancers to be linked epidemiologically to a definite risk factor, the underlying mechanisms of HCC pathogenesis remain unclear (4). The risk factors for HCC vary by location. In China, Hepatitis B or Hepatitis C virus infections are the main risk factors (5). The survival rate of patients with HCC has been extended due to progress in liver transplantation and other treatments; however, the insensitivity of chemotherapeutic drugs, cancer recurrence and metastasis continue to contribute to a poor prognosis (6). Thus, the identification of therapeutic targets and translation of molecular studies of HCC into clinical practice is urgently required.MicroRNAs (miRNAs) are a class of small non-coding RNAs, which are ~22 nucleotides in length (7-9). A number of miRNAs have been revealed to be involved in the pathogenesis of HCC (10-26). The roles of miR-1271 in numerous types of cancers have previously been investigated. For example, in gastric cancer, miR-1271 inhibited cell proliferation, invasion and epithelial-mesenchymal transition (EMT) by targeting forkhead box Q1 (FOXQ1) (27). Additionally, in oral squamous cell carcinoma, miR-1271 inhibited cell growth and metastasis by targeting anaplastic lymphoma receptor tyrosine kinase (28). In HCC, a previous study demonstrated that miR-96, miR-129-1-3p, miR-1291, miR-1303 and miR-1271 differentially regulated Glypican-3 (GPC3) expression levels in HCC cells and that the upregulation of GPC3 was associated with a concomitant downregulation of its repressor miR-1271 (29). However, the roles served by miR-1271 in HCC remain unclear.The present study analyzed the expression level of miR-1271 in HCC tissues and determined the in vitro function of miR-1271. The aim of the ...

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Section: Discussionmentioning

confidence: 99%

MicroRNA‑1271 inhibits cellular proliferation of hepatocellular carcinoma

et al. 2017

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“…Overall, miR-506 may be a promising miRNA for targeting FOXQ1. In addition, miR-124 is reportedly capable of targeting and inhibiting FOXQ1 to suppress tumor growth and metastasis in nasopharyngeal cancer (27). Zhang et al (26) reported that FOXQ1 is a target gene of miR-422a and that the overexpression of miR-422a inhibited the proliferation and migration of hepatocellular carcinoma.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have reported that FOXQ1 expression can be regulated by specific miRNAs in cancers (26,27). Bioinformatic research revealed that FOXQ1 has a putative binding site for miR-506 (Fig.…”

Section: Foxq1 Is a Potential Target Of Mir-506mentioning

confidence: 99%

Suppression of forkhead box Q1 by microRNA-506 represses the proliferation and epithelial-mesenchymal transition of cervical cancer cells

Zhang

Yan

et al. 2016

Oncology Reports

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Abstract. MicroRNAs (miRNAs) play a pivotal role in cancer progression and development, representing novel therapeutic tools for cancer therapy. Forkhead box Q1 (FOXQ1) functions as an oncogene in various cancer types. However, the functional significance of FOXQ1 in cervical cancer remains unknown. In this study, we investigated the biological function of FOXQ1 in cervical cancer and tested whether or not FOXQ1 can be targeted and regulated by specific miRNAs. We found that FOXQ1 was highly expressed in cervical cancer cell lines. Knockdown of FOXQ1 by small interfering RNA (siRNA) significantly suppressed the proliferation and epithelial-mesenchymal transition (EMT) of cervical cancer cells. FOXQ1 was predicted as a target gene of microRNA-506 (miR-506), and this prediction was validated by dual-luciferase reporter assay. Quantitative real-time PCR and western blot analyses demonstrated that mRNA and protein expression was negatively regulated by miR-506. The expression of miR-506 was downregulated in cervical cancer tissues, and miR-506 expression was inversely correlated with FOXQ1 expression in cervical cancer. The overexpression of miR-506 dramatically suppressed the proliferation and EMT of cervical cancer cells that mimicked the suppression of FOXO1 siRNA. Furthermore, the restoration of FOXQ1 expression significantly reversed the inhibitory effect of miR-506. Overall, our study demonstrated that miR-506 inhibited the proliferation and EMT of cervical cancer cells by targeting FOXQ1 and provided evidence that the miR-506/FOXQ1 axis plays an important role in the pathogenesis of cervical cancer, representing potential molecular targets for the development of anticancer agents for cervical cancer treatment.

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“…Эпигенетическое выключение 3 локусов miR-124 (miR-124-1 / 2 / 3) наблюдается не только в опухолях головного мозга, но и при раз-личных других типах рака, таких как рак толстой киш-ки (75 % случаев), молочной железы (32-50 %), легких (48 %), лейкозе (36 %) и лимфоме (41 %). В контексте ОГШ рядом авторов был описан антипролифератив-ный эффект miR-124 [66,67], что указывает на возмож-ность аналогичного феномена угнетения синтеза этой молекулы в процессе развития плоскоклеточного рака.…”

Section: Introductionunclassified