The Antitumor Effect of TPD52L2 Silencing on Oxaliplatin-Resistant Gastric Carcinoma Is Related to Endoplasmic Reticulum Stress In Vitro

Zhang, Yu; Yang, Dejun; Wei, Ziran; Zhang, Xin; Hu, Zunqi; Fu, Hongbing; Xu, Jiapeng; Wang, Weijun

doi:10.1155/2022/4451178

Cited by 1 publication

(2 citation statements)

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“…A slowed tumor progression or a significantly increased apoptosis was reported upon MKI67 knockdown/knockout in several cancer cells lines [ 98 ]. Tumor protein D52-like 2 (TPD52L2/TPD54) was cited as overexpressed in BC, OC and PCa [ 63 ]. Its silencing, also identified in overexpressed JTB condition in this experiment, reduced cell viability, cell colony-forming potency, cell growth, and induces apoptosis and ER stress of oxaliplatin-resistant gastric carcinoma cells [ 63 ].…”

Section: Resultsmentioning

confidence: 99%

“…Tumor protein D52-like 2 (TPD52L2/TPD54) was cited as overexpressed in BC, OC and PCa [ 63 ]. Its silencing, also identified in overexpressed JTB condition in this experiment, reduced cell viability, cell colony-forming potency, cell growth, and induces apoptosis and ER stress of oxaliplatin-resistant gastric carcinoma cells [ 63 ]. JTB dysregulation in MCF7 cells was associated with downregulation of other proteins that might be associated with pro-apoptotic and anti-tumorigenic effects, such as calcium-calmodulin N-terminal domain 1(CALM1), downregulated here in overexpressed JTB condition, which induces apoptosis in MM cells [ 60 ] or ESCC [ 66 ], and SOD1, downregulated in both overexpressed and downregulated JTB condition [ 61 ].…”

Section: Resultsmentioning

confidence: 99%

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Investigating the Function of Human Jumping Translocation Breakpoint Protein (hJTB) and Its Interacting Partners through In-Solution Proteomics of MCF7 Cells

et al. 2022

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Human jumping translocation breakpoint (hJTB) gene is located on chromosome 1q21 and is involved in unbalanced translocation in many types of cancer. JTB protein is ubiquitously present in normal cells but it is found to be overexpressed or downregulated in various types of cancer cells, where this protein and its isoforms promote mitochondrial dysfunction, resistance to apoptosis, genomic instability, proliferation, invasion and metastasis. Hence, JTB could be a tumor biomarker for different types of cancer, such as breast cancer (BC), and could be used as a drug target for therapy. However, the functions of the protein or the pathways through which it increases cell proliferation and invasiveness of cancer cells are not well-known. Therefore, we aim to investigate the functions of JTB by using in-solution digestion-based cellular proteomics of control and upregulated and downregulated JTB protein in MCF7 breast cancer cell line, taking account that in-solution digestion-based proteomics experiments are complementary to the initial in-gel based ones. Proteomics analysis allows investigation of protein dysregulation patterns that indicate the function of the protein and its interacting partners, as well as the pathways and biological processes through which it functions. We concluded that JTB dysregulation increases the epithelial-mesenchymal transition (EMT) potential and cell proliferation, harnessing cytoskeleton organization, apical junctional complex, metabolic reprogramming, and cellular proteostasis. Deregulated JTB expression was found to be associated with several proteins involved in mitochondrial organization and function, oxidative stress (OS), apoptosis, and interferon alpha and gamma signaling. Consistent and complementary to our previous results emerged by using in-gel based proteomics of transfected MCF7 cells, JTB-related proteins that are overexpressed in this experiment suggest the development of a more aggressive phenotype and behavior for this luminal type A non-invasive/poor-invasive human BC cell line that does not usually migrate or invade compared with the highly metastatic MDA-MB-231 cells. This more aggressive phenotype of MCF7 cells related to JTB dysregulation and detected by both in-gel and in-solution proteomics could be promoted by synergistic upregulation of EMT, Mitotic spindle and Fatty acid metabolism pathways. However, in both JTB dysregulated conditions, several downregulated JTB-interacting proteins predominantly sustain antitumor activities, attenuating some of the aggressive phenotypical and behavioral traits promoted by the overexpressed JTB-related partners.

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Section: Resultsmentioning

confidence: 99%