MicroRNA-221-3p, a TWIST2 target, promotes cervical cancer metastasis by directly targeting THBS2

Wei, W.; Zhou, Chenfei; Wu, Xinglong; He, Lina; Wu, Lan-Fang; Chen, Xiaojing; Yan, Rong; Zhong, Ming; Yu, Yang; Li, Liang; Wang, Wei

doi:10.1038/s41419-017-0077-5

Cited by 98 publications

(65 citation statements)

References 43 publications

(44 reference statements)

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“…Bioinformatics analysis ( http://starbase.sysu.edu.cn/ ) found that miR-221 was the target of GAS5. Increasing evidence has shown that miR-221 promotes carcinogenesis, including cervical cancer, 24 osteosarcoma, 20 and lung cancer. 25 We found that miR-221 was upregulated in both PC tissues and cell lines ( Figures 1 C and 1D).…”

Section: Resultsmentioning

confidence: 99%

lncRNA GAS5 Reverses EMT and Tumor Stem Cell-Mediated Gemcitabine Resistance and Metastasis by Targeting miR-221/SOCS3 in Pancreatic Cancer

Liu

et al. 2018

Molecular Therapy - Nucleic Acids

142

112

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Dysregulated long noncoding RNAs (lncRNAs) and microRNAs (miRNAs) mediating chemotherapeutic drug effects and metastasis in pancreatic cancer (PC) are key reasons for the poor prognosis of this disease. lncRNA growth arrest-specific 5 (GAS5) is reported to be a tumor suppressor in multiple cancers. However, the functions of GAS5 and its related miRNAs in PC are poorly understood. This study explored the potential functions and mechanisms of GAS5 in PC gemcitabine resistance and metastasis. The results show that overexpression of GAS5 suppressed the proliferation, migration, gemcitabine resistance, stem cell-like properties, and epithelial-mesenchymal transition (EMT) of PC cells by directly binding to and suppressing miR-221 expression and enhancing suppressor of cytokine signaling 3 (SOCS3) expression. The effects of miR-221 overexpression on proliferation, migration, gemcitabine resistance, stem cell-like properties, and EMT inhibition were reversed by SOCS3 overexpression in PC cells. Additionally, GAS5 promoted gemcitabine-induced tumor growth and metastasis inhibition, as determined by Ki-67 staining and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), bioluminescence imaging, and the detection of cell-like properties and EMT in vivo. Thus, lncRNA GAS5 functioned as a competing endogenous RNA for miR-221, and it suppressed cell growth, metastasis, and gemcitabine resistance in PC by regulating the miR-221/SOCS3 pathway mediating EMT and tumor stem cell self-renewal.

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Section: Resultsmentioning

confidence: 99%

lncRNA GAS5 Reverses EMT and Tumor Stem Cell-Mediated Gemcitabine Resistance and Metastasis by Targeting miR-221/SOCS3 in Pancreatic Cancer

Liu

et al. 2018

Molecular Therapy - Nucleic Acids

142

112

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“…MicroRNA-221/222 participates in the progression of many tumors and has been reported to be highly expressed in cervical cancer 47 – 50 . Besides, two studies have revealed that HMGA1 could affect the expression of miR-222 in lung cancer 41 , 51 .…”

Section: Resultsmentioning

confidence: 99%

HMGA1 exacerbates tumor growth through regulating the cell cycle and accelerates migration/invasion via targeting miR-221/222 in cervical cancer

Wang

et al. 2018

Cell Death Dis

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High-mobility group AT-hook1 (HMGA1, formerly HMG-I/Y), an architectural transcription factor, participates in a number of tumor biological processes. However, its effect on cervical cancer remains largely indistinct. In this study, we found that HMGA1 was generally overexpressed in cervical cancer tissues and was positively correlated with lymph node metastasis and advanced clinical stage. Via exogenously increasing or decreasing the expression of HMGA1, we showed that HMGA1 affected the proliferation, colony formation, migration and invasion of cervical cancer cells in vitro. Rescue experiments suggested that miR-221/222 could partly reverse HMGA1-mediated migration and invasion processes. Mechanistically, we discovered that HMGA1 accelerated the G1/S phase transition by regulating the expression of cyclin D1 and cyclin E1, which was consistent with the results of the in vivo experiment. Furthermore, we found that HMGA1 regulated the expression of the miR-221/222 cluster at the transcriptional level and that miR-221/222 targeted the 3′UTR of tissue inhibitor of metalloproteinases 3(TIMP3). We propose a fresh perspective that HMGA1 participates in the migration and invasion process via the miR-221/222-TIMP3-MMP2/MMP9 axis in cervical cancer. In summary, our study identified a critical role played by HMGA1 in the progression of cervical cancer and the potential mechanisms by which exerts its effects, suggesting that targeting HMGA1-related pathways could be conducive to the therapies for cervical cancer.

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“…The abnormal expression of miRNAs in tumors is a research hotspot in the field of oncology. A variety of miRNAs that regulate the biological behavior of cervical cells through different target genes and participate in the occurrence, invasion, and metastasis of cervical cancer have been observed to be expressed abnormally in cervical cancer [8][9][10].…”

Section: Introductionmentioning

confidence: 99%

lncRNA DLG1-AS1 Promotes Cell Proliferation by Competitively Binding with miR-107 and Up-Regulating ZHX1 Expression in Cervical Cancer

Xin

Huang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Recent studies have revealed that long non-coding RNAs (lncRNAs) are involved in the occurrence and development of various tumors, thereby attracting increasing attention from researchers. The important biological functions of lncRNAs have been recognized gradually, but their mechanism in cervical cancer remains unclear. Methods: Differentially expressed lncRNAs in cervical cancer and para-carcinoma tissues were identified by screening using an lncRNA array, and candidate lncRNAs were verified by quantitative real-time PCR. A series of bioinformatics and molecular biological methods were adopted to investigate the interactions among lncRNAs, microRNAs (miRNAs), and miRNA target genes in cervical cancer. Cell viability was measured using a Cell Counting Kit-8 assay. Results: DLG1-AS1 was the most significantly up-regulated lncRNA in cervical cancer tissues, and it was confirmed that cervical cancer patients with high DLG1-AS1 expression had a poor prognosis. Down-regulation of DLG1-AS1 expression suppressed the proliferation of cervical cancer cells. Further investigation revealed that DLG1-AS1 eliminated the inhibition of miR-107 on the expression of its target gene ZHX1 by competitively binding to miR-107. Moreover, rescue assays proved that the effect of DLG1-AS1 on the proliferation of cervical cancer cells was dependent on miR-107. Conclusion: DLG1-AS1/miR-107/ZHX1 can form a competitive endogenous RNA network that regulates the proliferation of cervical cancer cells, resulting in tumor progression.

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MicroRNA-221-3p, a TWIST2 target, promotes cervical cancer metastasis by directly targeting THBS2

Cited by 98 publications

References 43 publications

lncRNA GAS5 Reverses EMT and Tumor Stem Cell-Mediated Gemcitabine Resistance and Metastasis by Targeting miR-221/SOCS3 in Pancreatic Cancer

lncRNA GAS5 Reverses EMT and Tumor Stem Cell-Mediated Gemcitabine Resistance and Metastasis by Targeting miR-221/SOCS3 in Pancreatic Cancer

HMGA1 exacerbates tumor growth through regulating the cell cycle and accelerates migration/invasion via targeting miR-221/222 in cervical cancer

lncRNA DLG1-AS1 Promotes Cell Proliferation by Competitively Binding with miR-107 and Up-Regulating ZHX1 Expression in Cervical Cancer

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