Cancer Research on Prevention and Treatment    2022, Vol. 49 Issue (06) : 575-580     DOI: 10.3971/j.issn.1000-8578.2022.21.1097
|
Effects of Pin1 on Proliferation and Apoptosis of HepG2 Cells Under Endoplasmic Reticulum Stress
JIANG Mingting1,2, HUANG Jing1,2, ZHENG Shuping3
1. Institute for Translational Medicine, Fujian Medical University, Fuzhou 350122, China; 2. Fujian Key Laboratory for Translational Research in Cancer and Neurodegenerative Diseases, Fuzhou 350122, China; 3. Public Technology Service Center, Fujian Medical University, Fuzhou 350122, China
Download: PDF(6496 KB)   ( 93 )   HTML ()
Export: BibTeX | EndNote | Reference Manager | ProCite | RefWorks
Abstract Objective To investigate the expression of Pin1 protein in HepG2 cells under endoplasmic reticulum stress (ERS) and its effect on cell proliferation and apoptosis. Methods The THLE3 cells were treated with tunicamycin (TM) (TM group) or DMSO (DMSO group) for 48h. The HepG2 cells were treated with TM (TM group), ATRA(ATRA group), TM+ATRA (TM+ATRA group) or DMSO (DMSO group) for 48h. The protein levels of Bip and Pin1 were detected by Western blot, cell proliferation was detected by CCK-8 assay, and cell apoptosis was detected by flow cytometry. Results The expression of Bip both increased in THLE3 and HepG2 cells treated with TM, indicated that TM effectively induced ERS in cells. Compared with the DMSO group, the protein level of Pin1 in THLE3 cells in TM group was decreased with the increasing of TM concentration (P<0.001). In TM+ATRA group, with the increasing of TM concentration, the expression of Pin1 was decreased in HepG2 cells (P<0.01). The inhibitory rates was (29.33±4.73)% in HepG2 cells in TM group, significantly lower than (60.33±2.08)% in THLE3 cells in TM group (P<0.001). In TM+ATRA group, the growth inhibition rates was increased to (60.33±6.03)% in HepG2 cells. The apoptosis rate of THLE3 cells in TM group was (22.25±0.78)%, significantly higher than (3.57±0.31)% in DMSO group (P<0.01). The apoptosis rates of HepG2 cells in ATRA group and TM+ATRA group were significantly higher than that in the DMSO group ((10.03±0.49)% vs. (5.10±1.00)%, P<0.05 and (23.70±0.75)% vs. (5.10±1.00)%, P<0.01). Conclusion HepG2 cells resist ERS-induced apoptosis by maintaining Pin1 protein level. Reducing the protein level of Pin1 can significantly inhibit the cell proliferation and induce apoptosis.
Keywords Pin1      Hepatocellular carcinoma      Cell proliferation      Apoptosis      Endoplasmic reticulum stress     
ZTFLH:  R735.7  
Fund:Startup Fund for Scientific Research, Fujian Medical University (No. 2017XQ1004)
Issue Date: 16 June 2022
 Cite this article:   
JIANG Mingting,HUANG Jing,ZHENG Shuping. Effects of Pin1 on Proliferation and Apoptosis of HepG2 Cells Under Endoplasmic Reticulum Stress[J]. Cancer Research on Prevention and Treatment, 2022, 49(06): 575-580.
 URL:  
http://www.zlfzyj.com/EN/10.3971/j.issn.1000-8578.2022.21.1097
http://www.zlfzyj.com/EN/Y2022/V49/I06/575
Service
E-mail this article
E-mail Alert
RSS
Articles by authors
JIANG Mingting
HUANG Jing
ZHENG Shuping
[1] Almanza A, Carlesso A, Chintha C, et al. Endoplasmic
reticulum stress signalling- from basic mechanisms to clinical
applications[J]. FEBS J, 2019, 286(2): 241-278.
[2] Hu H, Tian M, Ding C, et al. The C/EBP Homologous Protein
(CHOP) Transcription Factor Functions in Endoplasmic
Reticulum Stress-Induced Apoptosis and Microbial Infection[J].
Front Immunol, 2019, 9: 3083.
[3] Chipurupalli S, Kannan E, Tergaonkar V, et al. Hypoxia Induced
ER Stress Response as an Adaptive Mechanism in Cancer[J]. Int J
Mol Sci, 2019, 20(3): 749.
[4] Oakes SA. Endoplasmic Reticulum Stress Signaling in Cancer
Cells[J]. Am J Pathol, 2020, 190(5): 934-946.
[5] Sisinni L, Pietrafesa M, Lepore S, et al. Endoplasmic Reticulum
Stress and Unfolded Protein Response in Breast Cancer: The
Balance between Apoptosis and Autophagy and Its Role in Drug
Resistance[J]. Int J Mol Sci, 2019, 20(4): 857.
[6] Siwecka N, Rozpedek W, Pytel D, et al. Dual role of Endoplasmic
Reticulum Stress-Mediated Unfolded Protein Response Signaling
Pathway in Carcinogenesis[J]. Int J Mol Sci, 2019, 20(18): 4354.
[7] Llovet JM, Kelley RK, Villanueva A, et al. Hepatocellular
carcinoma[J]. Nat Rev Dis Primers,2021, 7(1): 7.
[8] Villanueva A. Hepatocellular Carcinoma[J]. N Engl J Med, 2019,
380(15): 1450-1462.
[9] Fabregat I. Dysregulation of apoptosis in hepatocellular carcinoma
cells[J]. World J Gastroenterol, 2009, 15(5): 513-520.
[10] Wu XZ. New strategy of antiangiogenic therapy for hepatocellular
carcinoma[J]. Neoplasma, 2008, 55(6): 472-481.
[11 ] Yu JH, Im CY, Min SH. Function of PIN1 in Cancer Development
and Its Inhibitors as Cancer Therapeutics[J]. Front Cell Dev Biol,
2020, 8: 120.
[12] Pu W, Zheng Y, Peng Y. Prolyl Isomerase Pin1 in Human Cancer:
Function, Mechanism, and Significance[J]. Front Cell Dev Biol,
2020, 8: 168.
[13] Nakatsu Y, Matsunaga Y, Ueda K, et al. Development of Pin1 Inhibitors and their Potential as Therapeutic Agents[J]. Curr Med
Chem, 2020, 27(20): 3314-3329.
[14] Jeong K, Kim SJ, Oh Y, et al. p53 negatively regulates Pin1 expr‍ession under ER stress[J]. Biochem Biophys Res Commun,
2014, 454(4): 518-523.
[15] Bae JS, Noh SJ, Kim KM, et al. PIN1 in hepatocellular carcinoma
is associated with TP53 gene status[J]. Oncol Rep, 2016, 36(4):
2405-2411 .
[16] Lukas J, Pospech J, Oppermann C, et al. Role of endoplasmic
reticulum stress and protein misfolding in disorders of the liver
and pancreas[J]. Adv Med Sci, 2019, 64(2): 315-323.
[17] Zhang LJ, Chen S, Wu P, et al. Inhibition of MEK blocks GRP78
up-regulation and enhances apoptosis induced by ER stress in
gastric cancer cells[J]. Cancer Lett, 2009, 274(1): 40-46.
[18] Rampone B, Schiavone B, Martino A, et al. Current management
strategy of hepatocellular carcinoma[J]. World J Gastroenterol,
2009, 15(26): 3210-3216.
[19] Bukowski K, Kciuk M, Kontek R. Mechanisms of Multidrug
Resistance in Cancer Chemotherapy[J]. Int J Mol Sci, 2020,
21(9): 3233.
Related articles from Frontiers Journals
[1] CAO Guangwen. Theoretical Update of Cancer Evo-Dev and Its Role in Targeted Immunotherapy for Hepatocellular Carcinoma[J]. Cancer Research on Prevention and Treatment, 2022, 49(08): 747-755.
[2] ZHOU Zhipeng, YANG Mingzhu, CAI Mingqin, XUE Juandi, LYU Xiaoyun. Mechanism of Astragaloside IV on HepG2 Cells Based on Molecular Dynamics Simulation and Experimental Evaluation[J]. Cancer Research on Prevention and Treatment, 2022, 49(07): 655-661.
[3] ZHOU Silei, SUN Guanqun, ZENG Tanlun, CHENG Zhuo, LIANG Xijun. Expression and Prognostic Value of CK2α' in Hepatocellular Carcinoma[J]. Cancer Research on Prevention and Treatment, 2022, 49(07): 662-666.
[4] ZHOU Shi. Progress in Locoregional Interventional Therapy of Primary Hepatocellular Carcinoma[J]. Cancer Research on Prevention and Treatment, 2022, 49(06): 552-556.
[5] ZHENG Jianzhou, BAI Yu, QI Chunjian. LncRNA FENDRR Affect Proliferation, Migration and Apoptosis of Lung Squamous Cell Carcinoma H226 Cells via ERK/MAPK Signaling Pathway[J]. Cancer Research on Prevention and Treatment, 2022, 49(06): 563-568.
[6] XU Huan, WANG Guangli, LI Tingming, WANG Wei, DONG Dandan. Transcriptome Analysis of Inhibitory Effect of Astaxanthin Against HepG2 Cell Lines[J]. Cancer Research on Prevention and Treatment, 2022, 49(06): 581-584.
[7] WANG Jue, JIN Zongrui, WANG Wei, YI Qilin, WANG Jilong, ZHU Hai, XU Banghao, GUO Ya, WEN Zhang. Prognostic Role of Immune-related Genes in Hepatocellular Carcinoma[J]. Cancer Research on Prevention and Treatment, 2022, 49(06): 599-605.
[8] XU Shasha, HAN Xingmin. Research Advances on Application of 18F-FDG PET/CT in Clinical Diagnosis and Treatment of Hepatocellular Carcinoma[J]. Cancer Research on Prevention and Treatment, 2022, 49(05): 384-389.
[9] ZHANG Yan, ZHANG Hongrui, MENG Dandan, YI Zhenying, XU Zhiqiao. Effects of MRE11 on Apoptosis and Proliferation of Esophageal Squamous Cancer Cells[J]. Cancer Research on Prevention and Treatment, 2022, 49(05): 396-402.
[10] CUI Honglei, ZHANG Xiaodan, GUO Danfeng, YAN Zhiping, GUO Wenzhi, ZHANG Shuijun. Expression of ENO3 and Its Effect on Sensitivity of Hepatocellular Carcinoma Cells to Oxaliplatin[J]. Cancer Research on Prevention and Treatment, 2022, 49(05): 438-443.
[11] SUN Miaomiao, LIU Kai, WANG Tong, QIU Sen, ZHAO Zhihua, CHEN Kuisheng. Effect of RhoC Expression in Vascular Endothelial Cells on Proliferation and Invasion of Myeloma RPMI8226 Cells[J]. Cancer Research on Prevention and Treatment, 2022, 49(04): 299-303.
[12] ZHOU Yongjie, WANG Zhengfeng, YAN Jun, WANG Haiping, XU Wen, ZHOU Wence. Value of Preoperative Lactate Dehydrogenase-to-Albumin Ratio Combined with AFP in Evaluating Prognosis of Patients with Hepatocellular Carcinoma[J]. Cancer Research on Prevention and Treatment, 2022, 49(04): 347-351.
[13] TAO Changcheng, ZHANG Kai, RONG Weiqi, WU Jianxiong. Research Progress of Early Recurrence and Cut-off Time of Hepatocellular Carcinoma after Radical Hepatectomy[J]. Cancer Research on Prevention and Treatment, 2022, 49(04): 359-363.
[14] XIA Qisheng, DENG Tingting, XU Yaping, LIU Honglin, LIU Haoyuan. Inhibitory Effect of Loropetalum Chinense on Proliferation of Lung Adenocarcinoma A549 Cells[J]. Cancer Research on Prevention and Treatment, 2022, 49(03): 182-186.
[15] HU Xiaoshu, WEN Yiyang, YANG Jinhua. Effect of PTENP1 on Proliferation and Apoptosis of Colorectal Cancer Cells and Its Molecular Mechanism[J]. Cancer Research on Prevention and Treatment, 2022, 49(03): 192-196.
Viewed
Full text


Abstract

Cited

  Shared   
  Discussed