IMR Press / EJGO / Volume 42 / Issue 3 / DOI: 10.31083/j.ejgo.2021.03.2416
Open Access Original Research
Overexpression of SOCS4 inhibits proliferation and migration of cervical cancer cells by regulating JAK1/STAT3 signaling pathway
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1 Department of Gynecology, Changsha Maternal and Child Health Care Hospital, 410017 Changsha City, Hunan Province, China
2 Department of Internal Medicine, Changsha Medical University, 410029 Changsha City, Hunan Province, China
3 Department of General Surgery, Changsha Maternal and Child Health Care Hospital, 410017 Changsha City, Hunan Province, China
Eur. J. Gynaecol. Oncol. 2021, 42(3), 554–560; https://doi.org/10.31083/j.ejgo.2021.03.2416
Submitted: 22 February 2021 | Revised: 17 March 2021 | Accepted: 26 March 2021 | Published: 15 June 2021
Abstract

Purpose: To delve into the related molecular mechanism of suppressor of cytokine signaling 4 (SOCS4) on cervical cancer cell proliferation and migration. Methods: Quantitative real-time polymerase chain reaction and western blot assays were employed to examine SOCS4 mRNA or protein expression in four human cervical cancer cell line (HeLa, SW-732, AV3, and CaSki) and normal cervical epithelium immortalized cell line (H8) MTT cell viability assays were applied to verify the cell proliferation of HeLa after overexpression of SOCS4. Wound scratch healing assays and transwell assays were applied to examine cell migration and invasion of HeLa after overexpression of SOCS4. Flow cytometry and western blot assays were applied to check the role of SOCS4 in the apoptosis of cervical cancer cells. The western blot assays were applied to examine the protein expression of JAK1, p-JAK1, STAT3, and p-STAT3 in HeLa after overexpression of SOCS4. Results: In this study, the results revealed that the mRNA and protein expression level of SOCS4 was lower in four human cervical cancer cell line than normal cervical epithelium immortalized cell line, respectively. Overexpression of SOCS4 inhibited the proliferation migration, and invasion of cervical cancer cells as well as promotes apoptosis of cervical cancer cells. Meanwhile, overexpression of SOCS4 in HeLa would inhibit phosphorylation of JAK1 and STAT3 protein. Conclusion: SOCS4 inhibited the proliferation and migration of cervical cancer cells by regulating the JAK1/STAT3 pathway.

Keywords
SOCS4
Cervical cancer
JAK1
STAT3
Figures
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