Tags

Type your tag names separated by a space and hit enter

Overexpression of the long non-coding RNA SPRY4-IT1 promotes tumor cell proliferation and invasion by activating EZH2 in hepatocellular carcinoma.
Biomed Pharmacother 2017; 85:348-354BP

Abstract

BACKGROUND

Increasing evidences have demonstrated that the dysregulation of long non-coding RNAs (lncRNAs) may act as an important role in tumor progression. The long non-coding RNA SPRY4 intronic transcript 1 (SPRY4-IT1) has been reported in some cancer including regulating cell growth, differentiation, apoptosis, and cancer progression. However, the expression and function of SPRY4-IT1 in the progression of hepatocellular carcinoma (HCC) remain largely unknown.

METHODS

The lncRNA SPRY4-IT1 was detected by quantitative real time PCR (qRT-PCR) in HCC cell lines, CCK8 cell proliferation and transwell invasion assays were performed to detect the GC cell proliferation and invasion abilities. The protein expression of E-cadherin, Vimentin and Twist1 was analyzed by Western blotting assays. Furthermore, RNA immunoprecipitation (RIP) and Chromatin immunoprecipitation (ChIP) assays were used to analyze potential molecular mechanism of SPRY4-IT1 in HCC cells.

RESULTS

We found that SPRY4-IT1 was up-regulated in HCC cell lines. Further function analysis demonstrated that knockdown of SPRY4-IT1 significantly inhibited HCC cells proliferation and invasion, but over-expression of SPRY4-IT1 had the opposite effects on HCC cells in vitro. Moreover, our results also indicated that SPRY4-IT1 over-expression significantly promoted the epithelial-mesenchymal transition (EMT) by up-regulating the transcription factor Twist1 and EMT marker Vimentin and inhibited the E-cadherin expression in MHCC97L cell. Whereas, knockdown of SPRY4-IT1 suppressed the transcription factor Twist1 and EMT marker Vimentin and increased the E-cadherin expression in MHCC97H cells. Mechanisms investigations showed that SPRY4-IT1 interacted with the EZH2 and epigenetically repressed the E-cadherin expression. In vivo, we also demonstrated that the tumor growth was inhibited in SPRY4-IT1 knockdown group compared with the control group.

CONCLUSIONS

These results suggested that lncRNA SPRY4-IT1 might be considered as a therapeutic target in HCC.

Authors+Show Affiliations

Department of Hepatopancreatobillary Surgery Treatment Center, Taihe Hospital, Hubei University of Medicine, Shiyan 442000, Hubei Province, China.Division of Gastrointestinal Surgery, Department of General Surgery, The Affiliated Huai'an Hospital of Xuzhou Medical University and The Second People's Hospital of Huai'an, Huai'an, China. Electronic address: zhangxiaoyu_ey@163.com.Department of Gastroenterology, Long gang District Central Hospital of Shenzhen, No. 6082 Long gang Avenue, Long gang District, Shenzhen, Guangdong, China. Electronic address: yuxi_8@aliyun.com.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

27899259

Citation

Zhou, Meng, et al. "Overexpression of the Long Non-coding RNA SPRY4-IT1 Promotes Tumor Cell Proliferation and Invasion By Activating EZH2 in Hepatocellular Carcinoma." Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie, vol. 85, 2017, pp. 348-354.
Zhou M, Zhang XY, Yu X. Overexpression of the long non-coding RNA SPRY4-IT1 promotes tumor cell proliferation and invasion by activating EZH2 in hepatocellular carcinoma. Biomed Pharmacother. 2017;85:348-354.
Zhou, M., Zhang, X. Y., & Yu, X. (2017). Overexpression of the long non-coding RNA SPRY4-IT1 promotes tumor cell proliferation and invasion by activating EZH2 in hepatocellular carcinoma. Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie, 85, pp. 348-354. doi:10.1016/j.biopha.2016.11.035.
Zhou M, Zhang XY, Yu X. Overexpression of the Long Non-coding RNA SPRY4-IT1 Promotes Tumor Cell Proliferation and Invasion By Activating EZH2 in Hepatocellular Carcinoma. Biomed Pharmacother. 2017;85:348-354. PubMed PMID: 27899259.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Overexpression of the long non-coding RNA SPRY4-IT1 promotes tumor cell proliferation and invasion by activating EZH2 in hepatocellular carcinoma. AU - Zhou,Meng, AU - Zhang,Xiao-Yu, AU - Yu,Xi, Y1 - 2016/11/28/ PY - 2016/10/13/received PY - 2016/11/08/accepted PY - 2016/12/3/pubmed PY - 2017/2/14/medline PY - 2016/12/1/entrez KW - EZH2 KW - Epithelial-mesenchymal transition KW - Hepatocellular carcinoma KW - SPRY4-IT1 SP - 348 EP - 354 JF - Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie JO - Biomed. Pharmacother. VL - 85 N2 - BACKGROUND: Increasing evidences have demonstrated that the dysregulation of long non-coding RNAs (lncRNAs) may act as an important role in tumor progression. The long non-coding RNA SPRY4 intronic transcript 1 (SPRY4-IT1) has been reported in some cancer including regulating cell growth, differentiation, apoptosis, and cancer progression. However, the expression and function of SPRY4-IT1 in the progression of hepatocellular carcinoma (HCC) remain largely unknown. METHODS: The lncRNA SPRY4-IT1 was detected by quantitative real time PCR (qRT-PCR) in HCC cell lines, CCK8 cell proliferation and transwell invasion assays were performed to detect the GC cell proliferation and invasion abilities. The protein expression of E-cadherin, Vimentin and Twist1 was analyzed by Western blotting assays. Furthermore, RNA immunoprecipitation (RIP) and Chromatin immunoprecipitation (ChIP) assays were used to analyze potential molecular mechanism of SPRY4-IT1 in HCC cells. RESULTS: We found that SPRY4-IT1 was up-regulated in HCC cell lines. Further function analysis demonstrated that knockdown of SPRY4-IT1 significantly inhibited HCC cells proliferation and invasion, but over-expression of SPRY4-IT1 had the opposite effects on HCC cells in vitro. Moreover, our results also indicated that SPRY4-IT1 over-expression significantly promoted the epithelial-mesenchymal transition (EMT) by up-regulating the transcription factor Twist1 and EMT marker Vimentin and inhibited the E-cadherin expression in MHCC97L cell. Whereas, knockdown of SPRY4-IT1 suppressed the transcription factor Twist1 and EMT marker Vimentin and increased the E-cadherin expression in MHCC97H cells. Mechanisms investigations showed that SPRY4-IT1 interacted with the EZH2 and epigenetically repressed the E-cadherin expression. In vivo, we also demonstrated that the tumor growth was inhibited in SPRY4-IT1 knockdown group compared with the control group. CONCLUSIONS: These results suggested that lncRNA SPRY4-IT1 might be considered as a therapeutic target in HCC. SN - 1950-6007 UR - https://www.unboundmedicine.com/medline/citation/27899259/Overexpression_of_the_long_non_coding_RNA_SPRY4_IT1_promotes_tumor_cell_proliferation_and_invasion_by_activating_EZH2_in_hepatocellular_carcinoma_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0753-3322(16)31909-6 DB - PRIME DP - Unbound Medicine ER -