Investigation of inhibition effect of daidzein on osteosarcoma cells based on experimental validation and systematic pharmacology analysis

Objective This study aims to explore the effect of daidzein, which is a natural isoflavone compound mainly extracted from soybeans, on osteosarcoma and the potential molecular mechanism. Material and Methods 143B and U2OS osteosarcoma cells were treated with gradient concentrations of daidzein, and MTT assay was used to determine the cell proliferation capacity and IC50. Hoechst 33342 staining and Annexin V-FITC/PI detection were used to determine apoptosis. Cell cycle was analyzed by flow cytometry, and migration ability were detected by transwell assays and scratch wound assay. An osteosarcoma xenograft mice model was applied to investigate the effect of daidzein on osteosarcoma in vivo. Systematic pharmacology and molecular modeling analysis were applied to predict the target of daidzein to osteosarcoma, and the target Src was verified by western blotting. We also observed the effect of daidzein on cell proliferation and apoptosis of Src-overexpressing osteosarcoma cells. Results In vitro, daidzein significantly inhibited 143B and U2OS osteosarcoma cell proliferation and migration, and induced cell cycle arrest. In vivo, daidzein exerts antitumor effects in osteosarcoma xenograft mice. After systematic screening and analysis, Src-MAPK signaling pathway was predicted as the highest-ranked pathway. Western blot demonstrated that daidzein inhibited phosphorylation of the Src-ERK pathway in osteosarcoma cells. Also, overexpression of Src could partially reverse the inhibitory effects of daidzein on osteosarcoma cell proliferation. Conclusion Daidzein exerts an antitumor effect on osteosarcoma, and the mechanism may be through the Src-ERK pathway.

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Downregulation of UBE2T can enhance the radiosensitivity of osteosarcoma in vitro and in vivo

Epigenomics ◽

10.2217/epi-2019-0125 ◽

2019 ◽

Vol 11 (11) ◽

pp. 1283-1305

Author(s):

Lin Shen ◽

Kai Zhao ◽

Han Li ◽

Bin Ning ◽

Wenzhao Wang ◽

...

Keyword(s):

Cell Cycle ◽

Cell Proliferation ◽

Immunohistochemical Analysis ◽

Gene Expression Omnibus ◽

Osteosarcoma Cell ◽

M Phase ◽

And Migration ◽

Species Production

Aim: To investigate the effect of UBE2T gene on radiotherapy for osteosarcoma. Materials & methods: Gene Expression Omnibus database, RT-qPCR and immunohistochemical analysis were performed. Cell proliferation and cell cycle experiments were conducted after knockdown of UBE2T. Cell scratch, reactive oxygen species production and apoptosis experiments were conducted after the combination of radiotherapy and UBE2T silencing. Then the xenograft mode was further conducted. Results: UBE2T was highly expressed in human osteosarcoma. Suppression of UBE2T inhibited osteosarcoma cell proliferation and induced cell cycle arrest at the G2/M phase. Downregulation of UBE2T combined with radiation can substantially inhibit clonal formation and migration, and promote apoptosis of osteosarcoma cells in vitro and in vivo. Conclusion: UBE2T downregulation can enhance the radiosensitivity of osteosarcoma in vitro and in vivo.

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A VEGFR2 Antagonist Inhibits Cell Proliferation, Migration, and Invasion by Blocking the PI3K-Akt and MAPK Signaling Pathways in Thyroid Cancer

10.21203/rs.3.rs-625662/v1 ◽

2021 ◽

Author(s):

Chunhao Liu ◽

Zhao Liu ◽

Hao Zhao ◽

Yue Cao ◽

Yansong Lin ◽

...

Keyword(s):

Cell Proliferation ◽

Thyroid Cancer ◽

Cell Lines ◽

Mapk Signaling ◽

Vascular Endothelial ◽

Antitumor Effects ◽

Invasion And Migration ◽

And Migration ◽

Mapk Signaling Pathways

Abstract Background: Vascular endothelial growth factor receptor-2 (VEGFR2)-mediated signaling cascades are involved in proliferation, migration, survival, and permeability changes in vascular endothelial cells. It was thought that VEGFR2 antagonists exerted their antitumor effects by inhibiting angiogenesis in tumor tissues. However, some recent studies have found that they have significant direct antitumor effects in some tumors. The aim of this study was to explore the antitumor effects and mechanisms of VEGFR2 antagonists in thyroid cancer (TC).Methods: The antitumor efficacy of a VEGFR2 antagonist (apatinib) in TC cells was evaluated through a series of in vitro experiments, and xenograft models were used to test its in vivo antitumor activity. The antitumor mechanisms of the VEGFR2 antagonist were explored using western blotting and immunohistochemistry.Results: Compared with that in the normal human thyroid cell line HTori3, the expression of VEGFR2 in TC cell lines (including IHH4, BCPAP, TPC-1, C643, K1, and 8305C) was significantly increased, especially in the C643 and 8305C cell lines. VEGFR2 antagonist inhibited the proliferation of C643 and 8305C cells in a dose-dependent manner, significantly reduced the invasion and migration of these cells, induced G0/G1 phase arrest and promoted cancer cell apoptosis. Additionally, the antiproliferative effect of the VEGFR2 antagonist was significantly reduced after KDR gene knockdown. In vivo experiments showed that tumor growth in nude mice was significantly inhibited in response to apatinib. The western blot and immunohistochemistry results showed that the VEGFR2 antagonist significantly reduced the expression and phosphorylation of VEGFR2 and further inhibited the phosphorylation of the downstream molecules Akt and ERK1/2.Conclusions: The VEGFR2 antagonist inhibited cell proliferation, invasion and migration in TC by inhibiting the PI3K/Akt and MAPK signaling pathways and exerted direct antitumor effects. Thus, directly targeting VEGFR2 can be an effective strategy for TC expressing VEGFR2.

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Panax Notoginseng Saponins Exert Anti-osteosarcoma Effect by Inhibiting G0 / G1 Phase and Affecting p53-mediated Autophagy and Mitochondrial Apoptosis

10.21203/rs.3.rs-138936/v1 ◽

2021 ◽

Author(s):

Guangtao Han ◽

Ting Liu

Keyword(s):

Cell Cycle ◽

Panax Notoginseng ◽

Osteosarcoma Cell ◽

Osteosarcoma Cells ◽

Panax Notoginseng Saponins ◽

Active Components ◽

Invasion And Migration ◽

And Migration

Abstract BackgroundOsteosarcoma is the most common primary bone malignancy. Chemotherapy for osteosarcoma often induces severe complications to the patients. Thus, the identification of new effective antineoplastic agents with fewer side effects remain a necessity. Panax notoginseng saponins (PNS) were therapeutic active components of panax notoginseng and were reported taking the capability to inhibit the growth of several tumors in vitro and in vivo. However, its effect on osteosarcoma has not been studied. This study first investigated the effect of PNS on osteosarcoma cells.MethodsCCK-8 essay used to determine the appropriate working concentration of PNS on osteosarcoma,annixV-FITC/PI experiment used to measure the apoptosis of PNS on osteosarcoma, wound healing assay was used to detect the migration of PNS on osteosarcoma, cell invasiveness was measured by transwell essay,cell cycle was measured by PI,the expression of relative protein was shown by western blot.ResultsOur result indicated that PNS inhibited osteosarcoma cells’ proliferation, invasion and migration, promoted their apoptosis. Besides, PNS also increased mitochondrial membrane potential and the level of reactive oxygen species. Cell cycle of osteosarcoma was arrested in G0 / G1 phase after treatment with PNS. The expression of p53, and mitochondrial related apoptosis proteins were promoted; however, decreased autophagy in osteosarcoma cells with PNS treatment were observed.ConclusionTaking the above effect of PNS on osteosarcoma, PNS were of the potential therapeutic value for treatment of osteosarcoma.

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miR-636 inhibits EMT, cell proliferation and cell cycle of ovarian cancer by directly targeting transcription factor Gli2 involved in Hedgehog pathway

Cancer Cell International ◽

10.1186/s12935-020-01725-7 ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Jiong Ma ◽

Chunxia Zhou ◽

Xuejun Chen

Keyword(s):

Cell Cycle ◽

Cell Proliferation ◽

Protein Expression ◽

Signaling Pathway ◽

Luciferase Reporter ◽

Cell Proliferation And Migration ◽

Hh Signaling ◽

And Migration ◽

Proliferation And Migration

Abstract Background Hedgehog (Hh) signaling pathway, which is essential for cell proliferation and differentiation, is noted to be aberrantly activated in tumor from increasing studies in recent years. MicroRNAs (miRNAs) as an important non-coding RNA in cells have been proven to possess a regulatory role specific to the Hh signaling pathway. Here, in vitro and in vivo cellular/molecular experiments were adopted to clarify the regulatory mechanism linking miR-636 to the Hh signaling pathway in ovarian cancer (OVC). Methods Protein–protein interaction analysis was performed to identify the hub gene in the Hh pathway. TargetScan database was used to predict the potential upstream regulators for Gli2. qRT-PCR was performed to test the expression of miR-636, while Western blot was conducted to detect the expression of proteins related to the Hh pathway and epithelial-mesenchymal transition (EMT). For cell functional experiments, HO-8910PM OVC cell line was used. MTT assay and wound healing assay were used to measure the effect of miR-636 on cell proliferation and migration. Flow cytometry was carried out to examine the effect of miR-636 on cell cycle, and Western blot was used to identify the change in expression of Hh and EMT-related proteins. Dual-luciferase reporter gene assay was implemented to detect the targeting relationship between miR-636 and Gli2. Xenotransplantation models were established for in vivo examination. Results Gli2 was identified as the hub gene of the Hh pathway and it was validated to be regulated by miR-636 based on the data from TargetScan and GEO databases. In vitro experiments discovered that miR-636 was significantly lowly expressed in OVC cell lines, and overexpressing miR-636 significantly inhibited HO-8910PM cell proliferation, migration and induced cell cycle arrest in G0/G1 phase, while the inhibition of miR-636 caused opposite results. Dual-luciferase reporter gene assay revealed that Gli2 was the target gene of miR-636 in OVC. Besides, overexpressed miR-636 decreased protein expression of Gli2, and affected the expression of proteins related to the Hh signaling pathway and EMT. Rescue experiments verified that overexpression of Gli2 reversed the inhibitory effect of miR-636 on HO-8910PM cell proliferation and migration, and attenuated the blocking effect of miR-636 on cell cycle. The xenotransplantation experiment suggested that miR-636 inhibited cell growth of OVC by decreasing Gli2 expression. Besides, overexpressing Gli2 potentiated the EMT process of OVC cells via decreasing E-cadherin protein expression and increasing Vimentin protein expression, and it reversed the inhibitory effect of miR-636 on OVC cell proliferation in vivo. Conclusion miR-636 mediates the activation of the Hh pathway via binding to Gli2, thus inhibiting EMT, suppressing cell proliferation and migration of OVC. Trial registration: The experimental protocol was established, according to the ethical guidelines of the Helsinki Declaration and was approved by the Human Ethics Committee of The Second Affiliated hospital of Zhejiang University School of Medicine (IR2019001235). Written informed consent was obtained from individual or guardian participants.

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Positive feedback between lncRNA FLVCR1-AS1 and KLF10 may inhibit pancreatic cancer progression via the PTEN/AKT pathway

Journal of Experimental & Clinical Cancer Research ◽

10.1186/s13046-021-02097-0 ◽

2021 ◽

Vol 40 (1) ◽

Author(s):

Jiewei Lin ◽

Shuyu Zhai ◽

Siyi Zou ◽

Zhiwei Xu ◽

Jun Zhang ◽

...

Keyword(s):

Cell Cycle ◽

Pancreatic Cancer ◽

Cell Proliferation ◽

Cancer Progression ◽

Positive Feedback ◽

Molecular Mechanisms ◽

Tumor Tissues ◽

And Migration

Abstract Background FLVCR1-AS1 is a key regulator of cancer progression. However, the biological functions and underlying molecular mechanisms of pancreatic cancer (PC) remain unknown. Methods FLVCR1-AS1 expression levels in 77 PC tissues and matched non-tumor tissues were analyzed by qRT-PCR. Moreover, the role of FLVCR1-AS1 in PC cell proliferation, cell cycle, and migration was verified via functional in vitro and in vivo experiments. Further, the potential competitive endogenous RNA (ceRNA) network between FLVCR1-AS1 and KLF10, as well as FLVCR1-AS1 transcription levels, were investigated. Results FLVCR1-AS1 expression was low in both PC tissues and PC cell lines, and FLVCR1-AS1 downregulation was associated with a worse prognosis in patients with PC. Functional experiments demonstrated that FLVCR1-AS1 overexpression significantly suppressed PC cell proliferation, cell cycle, and migration both in vitro and in vivo. Mechanistic investigations revealed that FLVCR1-AS1 acts as a ceRNA to sequester miR-513c-5p or miR-514b-5p from the sponging KLF10 mRNA, thereby relieving their suppressive effects on KLF10 expression. Additionally, FLVCR1-AS1 was shown to be a direct transcriptional target of KLF10. Conclusions Our research suggests that FLVCR1-AS1 plays a tumor-suppressive role in PC by inhibiting proliferation, cell cycle, and migration through a positive feedback loop with KLF10, thereby providing a novel therapeutic strategy for PC treatment.

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Degradation of long non-coding RNA-CIR decelerates proliferation, invasion and migration, but promotes apoptosis of osteosarcoma cells

Cancer Cell International ◽

10.1186/s12935-019-1076-7 ◽

2019 ◽

Vol 19 (1) ◽

Cited By ~ 1

Author(s):

Shiwei Liu ◽

Jingchao Li ◽

Liang Kang ◽

Yueyang Tian ◽

Yuan Xue

Keyword(s):

Tumor Growth ◽

Osteosarcoma Cell ◽

Loss Of Function ◽

Osteosarcoma Cells ◽

Invasion And Migration ◽

Normal Tissues ◽

Novel Target ◽

And Migration

Abstract Background Over the years, long non-coding RNAs (lncRNAs) have been clarified in malignancies, this research was focused on the role of lncRNA cartilage injury-related (lncRNA-CIR) in osteosarcoma cells. Methods LncRNA-CIR expression in osteosarcoma tissues and cells, and adjacent normal tissues and normal osteoblasts was determined, then the relations between lncRNA-CIR expression and the clinicopathological features, and between lncRNA-CIR expression and the prognosis of osteosarcoma patients were analyzed. Moreover, the MG63 and 143B cells were treated with silenced or overexpressed lncRNA-CIR, and then the proliferation, invasion, migration and apoptosis of the cells were evaluated by gain- and loss-of-function approaches. The tumor growth, and proliferation and apoptosis of osteosarcoma cells in vivo were observed by subcutaneous tumorigenesis in nude mice. Results We have found that lncRNA-CIR was up-regulated in osteosarcoma tissues and cells, which was respectively relative to adjacent normal tissues and normal osteoblasts. The expression of lncRNA-CIR was evidently correlated with disease stages, distant metastasis and differentiation of osteosarcoma patients, and the high expression of lncRNA-CIR indicated a poor prognosis. Furthermore, the reduction of lncRNA-CIR could restrict proliferation, invasion and migration, but promote apoptosis of osteosarcoma cells in vitro. Meanwhile, inhibited lncRNA-CIR also restrained tumor growth and osteosarcoma cell proliferation, whereas accelerated apoptosis of osteosarcoma cells in vivo. Conclusion We have found in this study that the inhibited lncRNA-CIR could decelerate proliferation, invasion and migration, but accelerate apoptosis of osteosarcoma cells, which may provide a novel target for osteosarcoma treatment.

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Long noncoding RNA LINC01111 suppresses pancreatic cancer aggressiveness by regulating DUSP1 expression via microRNA-3924

Cell Death and Disease ◽

10.1038/s41419-019-2123-y ◽

2019 ◽

Vol 10 (12) ◽

Cited By ~ 11

Author(s):

Shutao Pan ◽

Ming Shen ◽

Min Zhou ◽

Xiuhui Shi ◽

Ruizhi He ◽

...

Keyword(s):

Cell Cycle ◽

Pancreatic Cancer ◽

Cell Proliferation ◽

Cell Invasion ◽

Molecular Mechanisms ◽

Invasion And Migration ◽

Cancer Aggressiveness ◽

And Migration

AbstractDysfunction in long noncoding RNAs (lncRNAs) is reported to participate in the initiation and progression of human cancer; however, the biological functions and molecular mechanisms through which lncRNAs affect pancreatic cancer (PC) are largely unknown. Here, we report a novel lncRNA, LINC01111, that is clearly downregulated in PC tissues and plasma of PC patients and acts as a tumor suppressor. We found that the LINC01111 level was negatively correlated with the TNM stage but positively correlated with the survival of PC patients. The overexpression of LINC01111 significantly inhibited cell proliferation, the cell cycle, and cell invasion and migration in vitro, as well as tumorigenesis and metastasis in vivo. Conversely, the knockdown of LINC01111 enhanced cell proliferation, the cell cycle, and cell invasion and migration in vitro, as well as tumorigenesis and metastasis in vivo. Furthermore, we found that high expression levels of LINC01111 upregulated DUSP1 levels by sequestering miR-3924, resulting in the blockage of SAPK phosphorylation and the inactivation of the SAPK/JNK signaling pathway in PC cells and thus inhibiting PC aggressiveness. Overall, these data reveal that LINC01111 is a potential diagnostic biomarker for PC patients, and the newly identified LINC01111/miR-3924/DUSP1 axis can modulate PC initiation and development.

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AdipoRon Affects Cell Cycle Progression and Inhibits Proliferation in Human Osteosarcoma Cells

Journal of Oncology ◽

10.1155/2020/7262479 ◽

2020 ◽

Vol 2020 ◽

pp. 1-12 ◽

Cited By ~ 2

Author(s):

Luigi Sapio ◽

Ersilia Nigro ◽

Angela Ragone ◽

Alessia Salzillo ◽

Michela Illiano ◽

...

Keyword(s):

Cell Cycle ◽

Cell Lines ◽

Molecular Mechanisms ◽

Childhood And Adolescence ◽

Osteosarcoma Cell ◽

Osteosarcoma Cells ◽

Antitumor Effects ◽

Human Osteosarcoma Cells ◽

U2os Cells ◽

The Impact

AdipoRon (AdipoR) is the first synthetic molecule acting as a selective and potent adiponectin receptor agonist. Recently, the possible pharmacological use of AdipoR in different pathological conditions has been addressed. Interestingly, initial evidence suggests that AdipoR may have anticancer properties in different preclinical models, such as pancreatic and ovarian cancer. To our knowledge, so far no research has been directed at determining the impact of AdipoR on osteosarcoma, the most aggressive and metastatic bone malignancy occurring in childhood and adolescence age. Here, we investigate the possible antitumor effects of AdipoR in osteosarcoma cell lines. MTT and cell growth curve assays clearly indicate that AdipoR inhibits, at different extents, proliferation in both U2OS and Saos-2 osteosarcoma cell lines, the latter being more sensitive. Moreover, flow cytometry-based assays point out a significant G0/G1 phase accumulation and a contemporary S phase decrease in response to AdipoR. Consistent with the different sensitivity, a strong subG1 appearance in Saos-2 after 48 and 72 hours of treatment is also observed. The investigation of the molecular mechanisms highlights a common and initial ERK1/2 activation in response to AdipoR in both Saos-2 and U2OS cells. Interestingly, a simultaneous and dramatic downregulation of p70S6K phosphorylation, one of the main targets of mTORC1 pathway, has also been observed in AdipoR-treated Saos-2, but not in U2OS cells. Importantly, a strengthening of AdipoR-induced effects was reported upon everolimus-mediated mTORC1 perturbation in U2OS cells. In conclusion, our findings provide initial evidence of AdipoR as an anticancer molecule differently affecting various signaling pathways involved in cell cycle and cell death in osteosarcoma cells and encourage the design of future studies to further understand its pattern of activities.

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miR-422a inhibits osteosarcoma proliferation by targeting BCL2L2 and KRAS

Bioscience Reports ◽

10.1042/bsr20170339 ◽

2018 ◽

Vol 38 (2) ◽

Cited By ~ 5

Author(s):

Hao Zhang ◽

Qian-Yun He ◽

Guang-Chao Wang ◽

Da-Ke Tong ◽

Ren-Kai Wang ◽

...

Keyword(s):

Cell Cycle ◽

Cell Cycle Arrest ◽

Underlying Mechanism ◽

Clinical Samples ◽

Osteosarcoma Cell ◽

Osteosarcoma Cells ◽

Induce Cell Cycle Arrest ◽

Cycle Arrest

Osteosarcoma is the most common primary malignant bone tumor in children and adolescents. However, the underlying mechanism of osteosarcoma carcinogenesis and progression remains unknown. In the present study, we evaluated the expression profile of miRNAs in osteosarcoma tissues and the adjacent normal tissues. We found that the expression of miR-422a was down-regulated in osteosarcoma tissues and cell lines. In addition, we observed significantly elevated levels of repressive H3K9me3 and H3K27me3 and decreased active H3K4me3 on the promote region of miR-422a in osteosarcoma cells and clinical samples. Furthermore, up-regulation of miR-422a exhibited both in vitro and in vivo anti-tumor effects by inhibiting osteosarcoma cell growth and inducing apoptosis and cell cycle arrest. We also found that miR-422a targeted BCL2L2 and KRAS and negatively regulated their protein expression. Furthermore, restoration of miR-422a and knockdown of BCL2L2 and KRAS promoted apoptosis and induce cell cycle arrest in osteosarcoma cells. Taken together, the present study demonstrates that miR-422a may serve as a tumor suppressor in osteosarcoma via inhibiting BCL2L2 and KRAS translation both in vitro and in vivo. Therefore, miR-422a could be developed as a novel therapeutic target in osteosarcoma.

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miR-636 Inhibits EMT, Cell Proliferation and Cell Cycle of Ovarian Cancer by Directly Targeting the Transcription Factor Gli2 of Hedgehog Pathway

10.21203/rs.3.rs-52894/v1 ◽

2020 ◽

Author(s):

Jiong Ma ◽

Chunxia Zhou ◽

Xuejun Chen

Keyword(s):

Cell Cycle ◽

Cell Proliferation ◽

Protein Expression ◽

Luciferase Reporter ◽

Luciferase Reporter Gene ◽

Cell Proliferation And Migration ◽

Gene Assay ◽

And Migration ◽

Proliferation And Migration

Abstract Objective: Ovarian cancer (OVC) is the fifth leading cause of cancer-related deaths in women and has a significant impact on physical and mental health of women. This study explores the molecular mechanism of miR-636 acting as a tumor suppressor in OVC in vitro and in vivo, and provides new insight into the treatment of OVC.Methods: Protein-protein interaction (PPI) analysis was performed to identify the hub gene in Hedgehog (Hh) pathway. TargetScan database was used to predict the upstream regulatory miRNAs of Gli2 to obtain the target miRNA. qRT-PCR was performed to test the expression of miR-636, while Western blot were conducted to detect the expression of Hh and EMT (epithelial-mesenchymal transition) related genes in OVC cell lines. MTT assay and wound healing assay were used to measure the effect of miR-636 on OVC cell proliferation and migration. Flow cytometry was carried out to examine the effect of miR-636 on cell cycle, and Western blot was used for identification of changes in expression of Hh and EMT related proteins. Dual-luciferase reporter gene assay was implemented to detect the targeted relationship between miR-636 and Gli2. The xenotransplantation model was used to detect the effect of miR-636 on OVC cell proliferation in vivo.Results: PPI interaction analysis found that Gli2 was the hub gene in Hh pathway. Based on TargetScan and GEO databases, Gli2 was found to be targeted regulated by the upstream miR-636. In vitro experiments discovered that miR-636 was significantly lowly expressed in OVC cell lines. Overexpressing miR-636 significantly inhibited HO-8910PM cell proliferation and migration abilities as well as induced cell cycle arrest in G0/G1 phase, while the inhibition of miR-636 promoted cell proliferation and migration abilities. Dual-luciferase reporter gene assay revealed that Gli2 was a target gene of miR-636. Besides, overexpressing miR-636 decreased protein expression of Gli2, while the inhibition of miR-636 increased protein expression of Gli2. Furthermore, the overexpression and inhibition of miR-636 both affected the expression of proteins related to Hh signaling pathway and EMT. Rescue experiments verified that overexpression of Gli2 reversed the inhibitory effect of miR-636 on HO-8910PM cell proliferation and migration abilities, and attenuated the blocking effect of miR-636 on HO-8910PM cell cycle. The xenotransplantation model suggested that miR-636 inhibited cell growth of OVC by decreasing Gli2 expression. Besides, overexpressing Gli2 potentiated the EMT process in OVC via decreasing E-cadherin protein expression and increasing Vimentin protein expression, and it reversed the inhibitory effect of miR-636 on OVC cell proliferation and migration abilities in vivo.Conclusion: miR-636 inhibits the Hh pathway activation via targeted binding to Gli2, thus inhibiting EMT, cell proliferation and migration in OVC.

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