Inhibition of monoacylglycerol lipase restrains proliferation, migration, invasion, tumor growth and induces apoptosis in cervical cancer

Abstract Background Radiation resistance is a major obstacle to the prognosis of cervical cancer (CC) patients. Many studies have confirmed that long non-coding RNAs (lncRNAs) are involved in the regulation of radiosensitivity of cancers. However, whether small nucleolar RNA host gene 12 (SNHG12) regulates the radiosensitivity of CC remains unknown. Methods Quantitative real-time polymerase chain reaction was used to measure the expression levels of SNHG12 and microRNA-148a (miR-148a). The radiosensitivity of cells was evaluated by clonogenic assay. Flow cytometry and caspase-3 activity assay were performed to assess the apoptosis ability and cell cycle distribution of cells. Besides, dual-luciferase reporter and RNA immunoprecipitation assay were used to verify the interaction between miR-148a and SNHG12 or cyclin-dependent kinase 1 (CDK1). Also, the protein levels of CDK1, CCND1 and γ-H2AX were detected by western blot analysis. Furthermore, in vivo experiments were conducted to verify the effect of SNHG12 on CC tumor growth. Ki-67 and TUNEL staining were employed to evaluate the proliferation and apoptosis rates in vivo. The hematoxylin and eosin (HE) staining were employed to evaluate the tumor cell morphology. Results SNHG12 was upregulated in CC tissues and cells, and its knockdown improved the radiosensitivity by promoting the radiation-induced apoptosis and cell cycle arrest of CC cells. Also, miR-148a could be sponged by SNHG12 and could target CDK1. MiR-148a inhibitor or CDK1 overexpression could invert the promotion effect of silenced-SNHG12 on CC radiosensitivity. Meanwhile, SNHG12 interference reduced the tumor growth of CC, increased miR-148a expression, and inhibited CDK1 level in vivo. Conclusion LncRNA SNHG12 promoted CDK1 expression to regulate the sensitivity of CC cells to radiation through sponging miR-148a, indicating that SNHG12 could be used as a potential biomarker to treat the radiotherapy resistance of CC patients.

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miR-22 inhibits tumor growth and metastasis by targeting ATP citrate lyase: evidence in osteosarcoma, prostate cancer, cervical cancer and lung cancer

Oncotarget ◽

10.18632/oncotarget.10020 ◽

2016 ◽

Vol 7 (28) ◽

pp. 44252-44265 ◽

Cited By ~ 71

Author(s):

Mei Xin ◽

Zhiguang Qiao ◽

Jing Li ◽

Jianjun Liu ◽

Shaoli Song ◽

...

Keyword(s):

Prostate Cancer ◽

Lung Cancer ◽

Cervical Cancer ◽

Tumor Growth ◽

Atp Citrate Lyase ◽

Citrate Lyase ◽

Tumor Growth And Metastasis

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Circular RNA hsa_circ_0043280 inhibits cervical cancer tumor growth and metastasis via miR-203a-3p/PAQR3 axis

Cell Death and Disease ◽

10.1038/s41419-021-04193-7 ◽

2021 ◽

Vol 12 (10) ◽

Author(s):

Chunyu Zhang ◽

Pan Liu ◽

Jiaming Huang ◽

Yuandong Liao ◽

Chaoyun Pan ◽

...

Keyword(s):

Cervical Cancer ◽

Tumor Growth ◽

Poor Prognosis ◽

Prognostic Biomarker ◽

Circular Rna ◽

Circular Rnas ◽

Inhibit Tumor Growth ◽

Cancer Tumor ◽

Tumor Growth And Metastasis

AbstractCircular RNAs (circRNAs) are known to act as key regulators in a variety of malignancies. However, the role of circRNAs in cervical cancer (CCa) remains largely unknown. Herein, we demonstrated that a circRNA derived from the TADA2A gene (hsa_circ_0043280) was significantly downregulated in CCa and that this reduction in expression was correlated with a poor prognosis. Furthermore, our results demonstrated that hsa_circ_0043280 functions as a tumor suppressor to inhibit tumor growth and metastasis in CCa. Mechanistically, hsa_circ_0043280 competitively sponges miR-203a-3p and prevents miR-203a-3p from reducing the levels of PAQR3. Collectively, our results demonstrate that hsa_circ_0043280 plays a pivotal role in the development and metastasis of CCa, thus suggesting that hsa_circ_0043280 has significant potential as a prognostic biomarker and a therapeutic target for CCa.

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MiR-218 Impairs Tumor Growth and Increases Chemo-Sensitivity to Cisplatin in Cervical Cancer

International Journal of Molecular Sciences ◽

10.3390/ijms131216053 ◽

2012 ◽

Vol 13 (12) ◽

pp. 16053-16064 ◽

Cited By ~ 39

Author(s):

Jiarui Li ◽

Zhang Ping ◽

Hui Ning

Keyword(s):

Cervical Cancer ◽

Tumor Growth

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Upregulation of Long Non-Coding RNA Small Nucleolar RNA Host Gene 12 Contributes to Cell Growth and Invasion in Cervical Cancer by Acting as a Sponge for MiR-424-5p

Cellular Physiology and Biochemistry ◽

10.1159/000488045 ◽

2018 ◽

Vol 45 (5) ◽

pp. 2086-2094 ◽

Cited By ~ 33

Author(s):

Jing Dong ◽

Qing Wang ◽

Li Li ◽

Zhang Xiao-jin

Keyword(s):

Cervical Cancer ◽

Tumor Growth ◽

Cancer Cells ◽

Host Gene ◽

Migration And Invasion ◽

Small Nucleolar Rna ◽

Cervical Cancer Cells ◽

Cancer Tissues ◽

Nucleolar Rna

Background/Aims: Cervical cancer, which is one of the most aggressive cancers affecting females, has high rates of recurrence and mortality. Small nucleolar RNA host gene 12 (SNHG12) is known to promote the progression of several cancers; however, its exact effects and molecular mechanisms in cervical cancer remain unknown. Methods: Real-time quantitative PCR was used to determine the expression level of SNHG12 in cervical cancer tissues and cell lines. Loss-of-function assays were performed to examine the effect of SNHG12 on the proliferation, apoptosis, migration and invasion of cervical cancer cells in vitro and tumor growth in vivo. Luciferase experiments were employed to explore the interactions between SNHG12 and miR-424-5p. Results: SNHG12 was found to be abnormally elevated in human cervical cancer tissues compared with paired adjacent normal tissues. Moreover, high SNHG12 expression in tumor tissues was significantly correlated with vascular involvement, lymph node metastasis, advanced FIGO stage and poor prognosis. Furthermore, the knockdown of SNHG12 was found to inhibit proliferation, migration and invasion of cervical cancer cells in vitro, and silencing SNHG12 was shown to suppress tumor growth in a nude mouse model. Mechanistic studies showed that SNHG12 functioned as an endogenous sponge for miR-424-5p, thereby downregulating the expression of miR-424-5p in cervical cancer. Furthermore, the inhibition of miR-424-5p in SNHG12-depleted cells partially reversed the effects on cervical cancer cell apoptosis, adhesion and invasion. Conclusion: In summary, our findings suggest that the tumor-promoting role of SNHG12 is to function as a molecular sponge, which negatively regulates miR-424-5p. These findings may provide a potent therapeutic target for cervical cancer.

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