Overexpression of lncRNA H19/miR-675 promotes tumorigenesis in head and neck squamous cell carcinoma

Guan, Guofang; Zhang, Dejun; Wen, Lianji; Ding, Xiaoyan; Liu, Yan; Yu, Duo‐Jiao; Su, Kai; Zhu, Lin; Guo, Yingyuan; Wang, Ke

doi:10.7150/ijms.16571

Cited by 63 publications

(55 citation statements)

References 31 publications

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“…Recent studies have found that long non‐coding RNAs (LncRNAs), a member of non‐coding RNA gene family, are dysregulated in laryngeal cancer tissues . More interestingly, several LncRNAs, such as HOTAIR, NEAT1 and H19, function as oncogenes to promote the tumorigenesis of laryngeal cancer. Therefore, identifying the role of LncRNAs in laryngeal cancer may bring a novel insight into the occurrence and development of laryngeal cancer.…”

Section: Introductionmentioning

confidence: 99%

LncRNA MEG3 inhibits cell proliferation and induces apoptosis in laryngeal cancer via miR‐23a/APAF‐1 axis

Zhang

Wang

et al. 2019

J Cellular Molecular Medi

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Long non‐coding RNA (LncRNA) MEG3 serves a regulatory role in the progression of several types of cancer, but the role of MEG3 in laryngeal cancer is still unknown. The aim of this study was to explore the regulatory role and mechanism of MEG3 in laryngeal cancer. MEG3 expression in 50 laryngeal cancer tissue samples was detected by reverse transcription‐quantitative polymerase chain reaction (RT‐qPCR). The effects of MEG3 overexpression on laryngeal cancer cells were investigated in vitro and in vivo. The mechanism of competitive endogenous RNA (ceRNA) was validated through luciferase reporter assay, RT‐qPCR and Western blotting. MEG3 was down‐regulated in laryngeal cancer tissues, and the low MEG3 expression was associated with advanced clinical stage. Additionally, MEG3 overexpression inhibited the proliferation and induced the apoptosis of laryngeal cancer cells in vitro and in vivo. Particularly, MEG3 bound to miR‐23a specifically and a reciprocal negative regulation existed between miR‐23a and MEG3. Moreover, MEG3 up‐regulated apoptotic protease activating factor‐1 (APAF‐1), a known miR‐23a's target, thereby leading to the activation of caspase‐9 and caspase‐3. Meanwhile, these activated effects were rescued by miR‐23a overexpression. In conclusion, the present study demonstrated that MEG3 functions as a novel tumour suppressive LncRNA in laryngeal cancer for the first time. Furthermore, MEG3 may act as a ceRNA to regulate APAF‐1 expression by competitive binding to miR‐23a, thereby regulating the progression of laryngeal cancer.

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Section: Introductionmentioning

confidence: 99%

LncRNA MEG3 inhibits cell proliferation and induces apoptosis in laryngeal cancer via miR‐23a/APAF‐1 axis

Zhang

Wang

et al. 2019

J Cellular Molecular Medi

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“…H19 is first reported to be overexpressed in bladder carcinoma and has been indicated as a predict marker in cancer (Fellig et al, ). Overexpression of H19 can induce HNSCC progression (Guan et al, ). H19 is reported to be increased in glioma tissue and suggests poor patient survival (Zhang et al, ).…”

Section: Introductionmentioning

confidence: 99%

H19 promotes non‐small‐cell lung cancer (NSCLC) development through STAT3 signaling via sponging miR‐17

Huang

Lei

et al. 2018

Journal Cellular Physiology

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LncRNAs can exhibit crucial roles in the development of multiple cancers, including non-small cell lung cancer (NSCLC). Currently, we investigated the role of lncRNA H19 in NSCLC. In our study, it was found that H19 was upregulated in A549 and H1299 cells compared to normal lung epithelial BEAS-2B cells. Meanwhile, we observed that miR-17 was downregulated in NSCLC cell lines. Inhibited H19 can suppress the growth, migration, and invasion of NSCLC cells and bioinformatics search was performed to predict the correlation between H19 and miR-17. Overexpression of miR-17 was able to inhibit the progression of NSCLC cells while reversely miR-17 inhibitors reversed this process. In addition, signal transducers and activators of transcription (STAT3), as an mRNA target of miR-17, was presented in our research. Moreover, we discovered that H19 demonstrated its biological functions via regulating miR-17 and STAT3 in vitro. Silencing H19 greatly increased STAT3 expression by sponging miR-19 in vitro. It was hypothesized that H19 may serve as a competing endogenous RNA (ceRNA) to modulate STAT3 by attaching miR-17 in lung cancer. In summary, our findings indicated that H19/miR-17/STAT3 axis participated in NSCLC development. H19 could be regarded as a significant prognostic biomarker in NSCLC progression.

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“…Increasing studies have demonstrated that lncRNAs are associated with the occurrence and development of a variety of cancers . Several lncRNAs, such as UCA1, H19, and PVT1, have been reported in human head and neck carcinoma . To identify the biological function of KCNQ1OT1 in MSSCC, we demonstrated KCNQ1OT1 was upregulated in MSSCC tissues and the IMC‐3 cell line for the first time.…”

Section: Discussionmentioning

confidence: 83%

“…[26][27][28] Several lncRNAs, such as UCA1, H19, and PVT1, have been reported in human head and neck carcinoma. [29][30][31] To identify the biological function of KCNQ1OT1 in MSSCC, we demonstrated KCNQ1OT1 was upregulated in MSSCC tissues and the IMC-3 cell line for the first time. By performing loss-of-function experiments, we discovered KCNQ1OT1 promoted cell proliferation, migration, and invasion in MSSCC.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA KCNQ1OT1 promotes proliferation, migration, and invasion in maxillary sinus squamous cell carcinoma by regulating miR‐204/EphA7 axis

Sun

et al. 2019

J of Cellular Biochemistry

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Long noncoding RNAs have been demonstrated to contribute to the development and progression of various cancers. However, the underlying regulatory mechanisms of KCNQ1OT1 in tumorigenesis of maxillary sinus squamous cell carcinoma (MSSCC) remain unknown. Herein, we found that KCNQ1OT1 expression was markedly upregulated in MSSCC tissues and MSSCC cell line (IMC‐3) by using quantitative reverse transcription‐polymerase chain reaction. Loss‐of‐function experiments revealed that the deletion of KCNQ1OT1 inhibited cell proliferation, migration, and invasion. Moreover, we confirmed KCNQ1OT1 could directly interact with miR‐204 by bioinformatic prediction and dual luciferase assay, and miR‐204 inhibitor markedly reversed MSSCC tumor phenotypes induced by shKCNQ1OT1. Finally, we demonstrated that KCNQ1OT1/miR‐204 facilitated MSSCC progression by regulating Eph receptor A7 (EphA7). Taken together, these results revealed a novel regulatory mechanism KCNQ1OT1/miR‐204/EphA7 axis, which could provide a new understanding of MSSCC tumorigenesis and develop potential targets for MSSCC therapy.

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Overexpression of lncRNA H19/miR-675 promotes tumorigenesis in head and neck squamous cell carcinoma

Cited by 63 publications

References 31 publications

LncRNA MEG3 inhibits cell proliferation and induces apoptosis in laryngeal cancer via miR‐23a/APAF‐1 axis

LncRNA MEG3 inhibits cell proliferation and induces apoptosis in laryngeal cancer via miR‐23a/APAF‐1 axis

H19 promotes non‐small‐cell lung cancer (NSCLC) development through STAT3 signaling via sponging miR‐17

Long noncoding RNA KCNQ1OT1 promotes proliferation, migration, and invasion in maxillary sinus squamous cell carcinoma by regulating miR‐204/EphA7 axis

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