» Articles » PMID: 33931585

Serum Deprivation-response Protein Induces Apoptosis in Hepatocellular Carcinoma Through ASK1-JNK/p38 MAPK Pathways

Overview
Journal Cell Death Dis
Date 2021 May 1
PMID 33931585
Citations 20
Authors
Affiliations
Soon will be listed here.
Abstract

Serum deprivation-response protein (SDPR), a phosphatidylserine-binding protein, which is known to have a promising role in caveolar biogenesis and morphology. However, its function in hepatocellular carcinoma (HCC) was still largely unknown. In this study, we discussed the characterization and identification of SDPR, and to present it as a novel apoptosis candidate in the incidence of HCC. We identified 81 HCC cases with lower SDPR expression in the tumor tissues with the help of qRT-PCR assay, and lower SDPR expression was potentially associated with poor prognostication. The phenotypic assays revealed that cell proliferation, invasion, and migration were profoundly connected with SDPR, both in vivo and in vitro. The data obtained from the gene set enrichment analysis (GSEA) carried out on the liver hepatocellular carcinoma (LIHC), and also The Cancer Genome Atlas (TCGA) findings indicated that SDPR was involved in apoptosis and flow cytometry experiments further confirmed this. Furthermore, we identified the interaction between SDPR and apoptosis signal-regulating kinase 1 (ASK1), which facilitated the ASK1 N-terminus-mediated dimerization and increased ASK1-mediated signaling, thereby activating the JNK/p38 mitogen-activated protein kinases (MAPKs) and finally enhanced cell apoptosis. Overall, this work identified SDPR as a tumor suppressor, because it promoted apoptosis by activating ASK1-JNK/p38 MAPK pathways in HCC.

Citing Articles

ZSCAN16 expedites hepatocellular carcinoma progression via activating TBC1D31.

Wang X, Xiao B, Zhong F, Zhou Y, Wang Q, Jiang J Cell Div. 2024; 19(1):31.

PMID: 39511655 PMC: 11546084. DOI: 10.1186/s13008-024-00135-9.


Ectoin attenuates cortisone-induced skin issues by suppression GR signaling and the UVB-induced overexpression of 11β-HSD1.

Xu D, Wu Y J Cosmet Dermatol. 2024; 23(12):4303-4314.

PMID: 39222375 PMC: 11626367. DOI: 10.1111/jocd.16516.


Examining the evidence for mutual modulation between m6A modification and circular RNAs: current knowledge and future prospects.

Tang X, Guo M, Zhang Y, Lv J, Gu C, Yang Y J Exp Clin Cancer Res. 2024; 43(1):216.

PMID: 39095902 PMC: 11297759. DOI: 10.1186/s13046-024-03136-2.


The role of m6A methylation in targeted therapy resistance in lung cancer.

Xue H, Ma Y, Guan K, Zhou Y, Liu Y, Cao F Am J Cancer Res. 2024; 14(6):2994-3009.

PMID: 39005690 PMC: 11236795. DOI: 10.62347/LXOS2662.


GLUD1 inhibits hepatocellular carcinoma progression via ROS-mediated p38/JNK MAPK pathway activation and mitochondrial apoptosis.

Zhao Q, Yu M, Li J, Guo Y, Wang Z, Hu K Discov Oncol. 2024; 15(1):8.

PMID: 38216781 PMC: 10786780. DOI: 10.1007/s12672-024-00860-1.


References
1.
Tobiume K, Saitoh M, Ichijo H . Activation of apoptosis signal-regulating kinase 1 by the stress-induced activating phosphorylation of pre-formed oligomer. J Cell Physiol. 2002; 191(1):95-104. DOI: 10.1002/jcp.10080. View

2.
Qin S, Cheng Y, Liang J, Shen L, Bai Y, Li J . Efficacy and safety of the FOLFOX4 regimen versus doxorubicin in Chinese patients with advanced hepatocellular carcinoma: a subgroup analysis of the EACH study. Oncologist. 2014; 19(11):1169-78. PMC: 4221370. DOI: 10.1634/theoncologist.2014-0190. View

3.
Rincon M, Davis R . Regulation of the immune response by stress-activated protein kinases. Immunol Rev. 2009; 228(1):212-24. DOI: 10.1111/j.1600-065X.2008.00744.x. View

4.
Fujino G, Noguchi T, Matsuzawa A, Yamauchi S, Saitoh M, Takeda K . Thioredoxin and TRAF family proteins regulate reactive oxygen species-dependent activation of ASK1 through reciprocal modulation of the N-terminal homophilic interaction of ASK1. Mol Cell Biol. 2007; 27(23):8152-63. PMC: 2169188. DOI: 10.1128/MCB.00227-07. View

5.
Lin J, Zhang J, Lin S, Chertow G . Design of a phase 2 clinical trial of an ASK1 inhibitor, GS-4997, in patients with diabetic kidney disease. Nephron. 2014; 129(1):29-33. DOI: 10.1159/000369152. View