LncRNA CEACAMP8 Regulates the Proliferation, Invasion and Migration of Trophoblast Cells

Preeclampsia (PE) is an idiopathic hypertension syndrome occurring after 20 weeks of gestation. Reports showed that lncRNAs expression was abnormal in preeclampsia. We aimed to investigate the role of lncRNA CEACAMP8 in the proliferation, invasion and migration of trophoblast cells to improve the preeclampsia. The cell transfection effects were determined by RT-qPCR analysis. The proliferation, invasion and migration of HTR-8/SVneo cells were detected by CCK-8 assay, transwell assay and wound healing assay. The flow cytometry analysis analyzed the cell cycle. Moreover, the expression of CDK2, cyclinD1, P21, MMP2, MMP9, E-cadherin, b-catenin and vimentin was determined by the western blot analysis. Consequently, CEACAMP8 inhibition promoted the proliferation, invasion and migration of HTR-8/SVneo cells and kept most of the cells in the S phase. The expression of proteins related to the proliferation, invasion and migration of HTR-8/SVneo cells were also changed in accordance with the increase of proliferation, invasion and migration of HTR-8/SVneo cells. In addition, lncRNA CEACAMP8 inhibition decreased the expression of E-cadherin and b-catenin, and increased the vimentin expression to promote the epithelial-mesenchymal transition. And, CEACAMP8 overexpression could reverse the above changes. This study indicated that CEACAMP8 inhibition promoted the proliferation, invasion and migration of HTR-8/SVneo cells and lncRNA CEACAMP8 overexpression reversed.

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BK polyomavirus infection promotes growth and aggressiveness in bladder cancer

Virology Journal ◽

10.1186/s12985-020-01399-7 ◽

2020 ◽

Vol 17 (1) ◽

Cited By ~ 2

Author(s):

Yigang Zeng ◽

Jiajia Sun ◽

Juan Bao ◽

Tongyu Zhu

Keyword(s):

Bladder Cancer ◽

Signaling Pathway ◽

Epithelial Mesenchymal Transition ◽

Cell Model ◽

Mesenchymal Transition ◽

Invasion And Migration ◽

Urothelial Carcinomas ◽

Bk Polyomavirus ◽

And Migration

Abstract Background Recent studies have confirmed the integration of the BK polyomavirus (BKPyV) gene into the cellular genome of urothelial carcinomas in transplant recipients, further confirming the correlation between BKPyV and urothelial carcinomas after transplantation. However, the role BKPyV infections play in the biological function of bladder cancer remains unclear. Methods We developed a BKPyV-infected bladder cancer cell model and a mice tumor model to discuss the role of BKPyV infections. Results Our research proves that BKPyV infections promote the proliferation, invasion and migration of bladder cancer cells, while the activation of β-catenin signaling pathway is one of its mediation mechanisms. Conclusions We first described BKPyV infection promotes the proliferation, invasion and migration of bladder cancer. We verified the role of β-catenin signaling pathway and Epithelial-Mesenchymal Transition effect in BKPyV-infected bladder cancer. These results provide meaningful information towards the diagnosis and treatment of clinical bladder cancer.

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BK polyomavirus infection promotes growth and aggressiveness in bladder cancer

10.21203/rs.3.rs-27734/v1 ◽

2020 ◽

Author(s):

Jiajia Sun ◽

Yigang Zeng ◽

Juan Bao ◽

Tongyu Zhu

Keyword(s):

Bladder Cancer ◽

Signaling Pathway ◽

Epithelial Mesenchymal Transition ◽

Cell Model ◽

Mesenchymal Transition ◽

Invasion And Migration ◽

Urothelial Carcinomas ◽

Bk Polyomavirus ◽

And Migration

Abstract Background Recent studies have confirmed the integration of the BK polyomavirus (BKPyV) gene into the cellular genome of urothelial carcinomas in transplant recipients, further confirming the correlation between BKPyV and urothelial carcinomas after transplantation. However, the role BKPyV infections play in the biological function of bladder cancer remains unclear.Methods We developed a BKPyV-infected bladder cancer cell model and a mice tumor model to discuss the role of BKPyV infections.Results Our research proves that BKPyV infections promote the proliferation, invasion and migration of bladder cancer, while the activation of β-catenin signaling pathway is one of its mediation mechanisms.Conclusions We first described BKPyV infection promotes the proliferation, invasion and migration of bladder cancer. We verified the role of β-catenin signaling pathway and Epithelial-Mesenchymal Transition effect in BKPyV-infected bladder cancer. These results provide meaningful information towards the diagnosis and treatment of clinical bladder cancer.

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Hepatitis B virus X protein promotes vimentin expression via LIM and SH3 domain protein 1 to facilitate epithelial-mesenchymal transition and hepatocarcinogenesis

Cell Communication and Signaling ◽

10.1186/s12964-021-00714-1 ◽

2021 ◽

Vol 19 (1) ◽

Author(s):

Hongjuan You ◽

Dongchen Yuan ◽

Yanwei Bi ◽

Ning Zhang ◽

Qi Li ◽

...

Keyword(s):

Western Blot ◽

Epithelial Mesenchymal Transition ◽

Hepatoma Cells ◽

Signal Pathways ◽

Vimentin Expression ◽

Mesenchymal Transition ◽

B Virus ◽

And Migration ◽

The Stability

Abstract Background Hepatitis B virus (HBV) X protein (HBX) has been reported to be responsible for the epithelial-mesenchymal transition (EMT) in HBV-related hepatocellular carcinoma (HCC). Vimentin is an EMT-related molecular marker. However, the importance of vimentin in the pathogenesis of HCC mediated by HBX has not been well determined. Methods The expression of vimentin induced by HBX, and the role of LIM and SH3 domain protein 1 (LASP1) in HBX-induced vimentin expression in hepatoma cells were examined by western blot and immunohistochemistry analysis. Both the signal pathways involved in the expression of vimentin, the interaction of HBX with vimentin and LASP1, and the stability of vimentin mediated by LASP1 in HBX-positive cells were assessed by western blot, Co-immunoprecipitation, and GST-pull down assay. The role of vimentin in EMT, proliferation, and migration of HCC cells mediated by HBX and LASP1 were explored with western blot, CCK-8 assay, plate clone formation assay, transwell assay, and wound healing assay. Results Vimentin expression was increased in both HBX-positive hepatoma cells and HBV-related HCC tissues, and the expression of vimentin was correlated with HBX in HBV-related HCC tissues. Functionally, vimentin was contributed to the EMT, proliferation, and migration of hepatoma cells mediated by HBX. The mechanistic analysis suggested that HBX was able to enhance the expression of vimentin through LASP1. On the one hand, PI3-K, ERK, and STAT3 signal pathways were involved in the upregulation of vimentin mediated by LASP1 in HBX-positive hepatoma cells. On the other hand, HBX could directly interact with vimentin and LASP1, and dependent on LASP1, HBX was capable of promoting the stability of vimentin via protecting it from ubiquitination mediated protein degradation. Besides these, vimentin was involved in the growth and migration of hepatoma cells mediated by LASP1 in HBX-positive hepatoma cells. Conclusion Taken together, these findings demonstrate that, dependent on LASP1, vimentin is crucial for HBX-mediated EMT and hepatocarcinogenesis, and may serve as a potential target for HBV-related HCC treatment.

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IGF2BP2 Promotes the Proliferation, Invasion and Migration of Esophageal Carcinoma Cells via Activation of the PI3K/AKT/EMT Signaling Pathway

10.21203/rs.3.rs-711778/v1 ◽

2021 ◽

Author(s):

Wenbin Shu ◽

YuJing Lin ◽

Yan Yan ◽

YaoHui Sun ◽

XiangWen Wu ◽

...

Keyword(s):

Signaling Pathway ◽

Epithelial Mesenchymal Transition ◽

Akt Signaling ◽

Akt Signaling Pathway ◽

Mesenchymal Transition ◽

Invasion And Migration ◽

And Migration ◽

Mrna Binding

Abstract BackgroundInsulin-like growth factor 2 (IGF2) mRNA-binding protein 2 (IGF2BP2), as a m6A “reader”, is known to be an oncogene, and its expression is elevated in multiple tumors. However, the role of IGF2PB2 in esophageal squamous cell carcinoma (ESCC) is still unclear. MethodsThis study aims to investigate the role of IGF2PB2 expression in ESCC proliferation, invasion and migration as well as the possible mechanism. IGF2BP2 expression was found to be elevated in ESCC tissues by qRT-PCR, western blotting, and immunohistochemical (IHC) staining. ResultsKnocking down IGF2BP2 expression prevented the proliferation, invasion, migration and epithelial-mesenchymal transition (EMT) of KYSE450 and TE1 cells. Knocking out IGF2BP2 reduced tumorigenesis in vivo. Overexpression of IGF2BP2 was performed, and it was proven that IGF2BP2 had an oncogenic effect in KYSE450 and TE1 cells. Moreover, LY294002, a highly selective inhibitor of PI3K, reversed the effect of IGF2BP2 overexpression on EMT processes. All these results show that the effects of IGF2BP2 on oncogenesis and EMT were clearly exerted via the PI3K/AKT signaling pathway. ConclusionsIn conclusion, this study demonstrates that the oncogenic function of IGF2BP2 is mediated by the PI3K/AKT signaling pathway and is related to EMT in ESCC. In addition, IGF2BP2 can serve as a diagnostic and oncotherapeutic marker in further studies.

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SDC1 knockdown induces epithelial–mesenchymal transition and invasion of gallbladder cancer cells via the ERK/Snail pathway

Journal of International Medical Research ◽

10.1177/0300060520947883 ◽

2020 ◽

Vol 48 (8) ◽

pp. 030006052094788

Author(s):

Zixiang Liu ◽

Hao Jin ◽

Song Yang ◽

Haiming Cao ◽

Ziyan Zhang ◽

...

Keyword(s):

Cell Proliferation ◽

Gallbladder Cancer ◽

Epithelial Mesenchymal Transition ◽

Negative Control ◽

Cell Counting ◽

Mesenchymal Transition ◽

Expression Levels ◽

Invasion And Migration ◽

And Migration ◽

E Cadherin

Background Expression levels of the cell adhesion molecule syndecan-1 (SDC1) have been shown to be inversely proportional to tumor differentiation and prognosis. However, its role in the development of gallbladder cancer (GBC) remains unclear. Methods We knocked down SDC1 in GBC cells by RNA interference and determined its roles in cell proliferation, apoptosis, invasion, and migration by Cell Counting Kit-8, colony-formation, flow cytometry, Hoechst 33342 staining, transwell invasion, and scratch wound assays. Expression levels of epithelial–mesenchymal transition (EMT)-related and extracellular signal-regulated kinase (ERK)/Snail pathway proteins were determined by western blotting and immunofluorescence. Results Cell proliferation, invasion, and migration were all increased in GBC cells with SDC1 knockdown, compared with cells in the blank control and negative control groups, but apoptosis was similar in all three groups. E-cadherin and β-catenin expression levels were significantly lower and N-cadherin, vimentin, p-ERK1/2, and Snail expression were significantly higher in the SDC1 knockdown group compared with both controls, while ERK1/2 levels were similar in all groups. Reduced E-cadherin and increased vimentin levels were confirmed by immunofluorescence. Conclusions SDC1 knockdown promotes the proliferation, invasion, and migration of GBC cells, possibly by regulating ERK/Snail signaling and inducing EMT and cancer cell invasion.

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BK polyomavirus infection promotes growth and aggressiveness in bladder cancer

10.21203/rs.3.rs-27734/v2 ◽

2020 ◽

Author(s):

Yigang Zeng ◽

Jiajia Sun ◽

Juan Bao ◽

Tongyu Zhu

Keyword(s):

Bladder Cancer ◽

Signaling Pathway ◽

Epithelial Mesenchymal Transition ◽

Cell Model ◽

Mesenchymal Transition ◽

Invasion And Migration ◽

Urothelial Carcinomas ◽

Bk Polyomavirus ◽

And Migration

Abstract Background: Recent studies have confirmed the integration of the BK polyomavirus (BKPyV) gene into the cellular genome of urothelial carcinomas in transplant recipients, further confirming the correlation between BKPyV and urothelial carcinomas after transplantation. However, the role BKPyV infections play in the biological function of bladder cancer remains unclear. Methods: We developed a BKPyV-infected bladder cancer cell model and a mice tumor model to discuss the role of BKPyV infections. Results: Our research proves that BKPyV infections promote the proliferation, invasion and migration of bladder cancer cells, while the activation of β-catenin signaling pathway is one of its mediation mechanisms. Conclusions: We first described BKPyV infection promotes the proliferation, invasion and migration of bladder cancer. We verified the role of β-catenin signaling pathway and Epithelial-Mesenchymal Transition effect in BKPyV-infected bladder cancer. These results provide meaningful information towards the diagnosis and treatment of clinical bladder cancer.

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Long Noncoding RNA HOST2 Promotes Epithelial-Mesenchymal Transition, Proliferation, Invasion and Migration of Hepatocellular Carcinoma Cells by Activating the JAK2-STAT3 Signaling Pathway

Cellular Physiology and Biochemistry ◽

10.1159/000495231 ◽

2018 ◽

Vol 51 (1) ◽

pp. 301-314 ◽

Cited By ~ 18

Author(s):

Yang Wu ◽

Tan Yuan ◽

Wei-Wei Wang ◽

Peng-Lei Ge ◽

Zhi-Qiang Gao ◽

...

Keyword(s):

Signaling Pathway ◽

Noncoding Rna ◽

Epithelial Mesenchymal Transition ◽

Migration And Invasion ◽

Mesenchymal Transition ◽

Invasion And Migration ◽

Stat3 Signaling ◽

Stat3 Signaling Pathway ◽

And Migration ◽

E Cadherin

Background/Aims: This study aims to examine the effect of long noncoding RNA HOST2 (LncRNA HOST2) on epithelial-mesenchymal transition (EMT), proliferation, invasion and migration of hepatocellular carcinoma (HCC) cells via activation of the JAK2-STAT3 signaling pathway. Methods: HCC and para-cancerous tissues were collected from 136 HCC patients. Immunohistochemistry was used to detect the expression of JAK2 and STAT3. HCC SMMC7721 cells were grouped into blank, negative control (NC), HOST2 mimic and HOST2 inhibitor groups. The mRNA and protein expression levels of HOST2, JAK2, STAT3, E-cadherin, vimentin, Snail, Slug, Twist and Zeb1 in tissues and cells were determined by reverse transcription -quantitative polymerase chain reaction (RT-qPCR) and Western blotting, respectively. An MTT assay, scratch test and Transwell assay were applied to measure cell proliferation, migration and invasion, respectively. Results: The levels of JAK2, STAT3 and vimentin were higher in HCC tissues, while the expression of E-cadherin was lower in HCC tissues compared with para-cancerous tissues. The silencing of HOST2 significantly decreased cell proliferation, migration and invasion, reduced the levels of HOST2, JAK2, STAT3 and vimentin, and elevated the expression of E-cadherin. HOST2 silencing also decreased the levels of Snail, Slug and Twist but increased the level of Zeb1 protein, while the opposite findings were observed in the HOST2 mimic group. Conclusion: These results reveal a possible mechanism in HCC in which LncRNA HOST2 may increase EMT and enhance proliferation, invasion and metastasis of HCC cells via activation of the JAK2-STAT3 signaling pathway.

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High STRN Expression Promotes HCC Invasion and Migration but Not Cell Proliferation or Apoptosis through Facilitating Epithelial-Mesenchymal Transition

BioMed Research International ◽

10.1155/2020/6152925 ◽

2020 ◽

Vol 2020 ◽

pp. 1-10

Author(s):

Qian-yu Du ◽

Jing-hao Yao ◽

Yong-chun Zhou ◽

Ling-jie Xu ◽

Fu-you Zhao ◽

...

Keyword(s):

Cell Proliferation ◽

Cell Invasion ◽

Tumour Cell ◽

Epithelial Mesenchymal Transition ◽

Morphological Changes ◽

Mesenchymal Transition ◽

Invasion And Migration ◽

Huh7 Cells ◽

And Migration ◽

E Cadherin

A STRN-ALK fusion protein has been recently identified as a potential therapeutic target in multiple cancers; however, the role of STRN alone in regulating the biological function of hepatocellular carcinoma (HCC) remains unclear. In this study, we firstly detected an overexpression of STRN in HCC tissues compared to that in adjacent nontumour (ANT) tissues through IHC analysis, and the expression level of this protein was positively correlated with lymph node metastasis and TNM stage. In vitro, high expression of STRN was also confirmed in different HCC cell lines, and regulation of STRN expression in Huh7 cells did not significantly affect tumour cell proliferation or apoptosis but was positively correlated with tumour cell invasion and migration capacities. Moreover, both the knockdown and overexpression of STRN in Huh7 cells can lead to cell morphological changes that are accompanied with an alteration of epithelial-mesenchymal transition (EMT) molecular markers E-cadherin and Vimentin. Finally, STRN was further proved to be negatively related to E-cadherin expression but positively related to Vimentin expression in human HCC tissue samples. Taken together, STRN is upregulated in HCC and acts as a tumour promoter regulating cell invasion and migration through facilitating the EMT process.

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Up-regulation of miR-34c-5p inhibits nasopharyngeal carcinoma cells by mediating NOTCH1

Bioscience Reports ◽

10.1042/bsr20200302 ◽

2020 ◽

Vol 40 (6) ◽

Author(s):

Xin Xu ◽

Haomin Yan ◽

Le Zhang ◽

Jing Liu ◽

Yu Huang ◽

...

Keyword(s):

Nasopharyngeal Carcinoma ◽

Biological Function ◽

Epithelial Mesenchymal Transition ◽

Carcinoma Cells ◽

Normal Cells ◽

Mesenchymal Transition ◽

Invasion And Migration ◽

Rescue Experiment ◽

And Migration

Abstract Objective: To explore the correlation between miR-34c-5p and NOTCH1 in nasopharyngeal carcinoma (NPC). Materials and methods: qPCR was employed to quantify miR-34c-5p and NOTCH1 mRNA in NPC, and Western blot to detect NOTCH1. MiR-34c-5p mimics/inhibitor and NOTCH1 siRNA were constructed to analyze the role of miR-34c-5p/NOTCH1 on the biological function of NPC cells. Results: NPC cells showed lower miR-34c-5p expression and higher NOTCH1 expression than normal cells, and up-regulating miR-34c-5p or inhibiting NOTCH1 could strongly suppress the epithelial–mesenchymal transition (EMT), proliferation, invasion and migration of NPC cells, and induce apoptosis in them. Up-regulating miR-34c-5p could inhibit NOTCH1, and miR-34c-5p was negatively correlated with NOTCH1. Rescue experiment results revealed that NOTCH1 up-regulation could counteract the changes of cell process induced by increased miR-34c-5p. Conclusion: MiR-34c-5p inhibits the growth of NPC by down-regulating NOTCH1, so up-regulating miR-34c-5p or down-regulating NOTCH1 may become the potential direction of NPC treatment.

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HOTAIR Contributes to Stemness Acquisition of Cervical Cancer through Regulating miR-203 Interaction with ZEB1 on Epithelial-Mesenchymal Transition

Journal of Oncology ◽

10.1155/2021/4190764 ◽

2021 ◽

Vol 2021 ◽

pp. 1-11

Author(s):

Wenying Zhang ◽

Jing Liu ◽

Qiongwei Wu ◽

Yu Liu ◽

Chengbin Ma

Keyword(s):

Cervical Cancer ◽

Stem Cells ◽

Cancer Stem Cells ◽

Cultured Cells ◽

Epithelial Mesenchymal Transition ◽

Mesenchymal Transition ◽

Invasion And Migration ◽

Cervical Cancer Cells ◽

And Migration

Cervical cancer stem cells contribute respond to considerable recurrence and metastasis of patients with cervical cancer. The stemness properties were partly regulated by the interaction of lncRNAs and miRNAs. HOTAIR functions as an oncogenic lncRNA. Previous research studies revealed its role in regulating stemness properties in various cancers. However, the role of HOTAIR in cervical cancer stem cells is still unknown. Here, cisplatin-resistant and serum-free cultured cells exhibited stem cells properties. Cervical cancer stem cells exhibited greater invasion and migration compared with their parental cells, which was similar to cells overexpressing HOTAIR. HOTAIR was significantly overexpressed in cervical cancer stem cells, and knockdown of HOTAIR generated statistical downregulation of stemness markers. Additionally, HOTAIR expression was negatively correlated with the level of miR-203, which was found to be an inhibitory miRNA in regulating the expressions of stemness markers. Also, miR-203 expression was negatively correlated with ZEB1. These findings suggested that HOTAIR should be a positive contributor in stemness acquisition of cervical cancer cells, and this effect should correlate with the interaction with miR-203, which can be suppressed by ZEB1.

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