cIAP2 via NF-κB signalling affects cell proliferation and invasion in hepatocellular carcinoma

Jiang, Xiaojie; Chen, Zhiwei; Zhao, Jianfeng; Liao, Changxi; Cai, Qing; Lin, Jing

doi:10.1016/j.lfs.2020.118867

Cited by 12 publications

(7 citation statements)

References 41 publications

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“…Cellular inhibitor of apoptosis (cIAP2) plays a role in degrading caspases by linking them to ubiquitin molecules and supports cell survival by preventing cellular apoptosis of cancer cells (41). cIAP-2 is upregulated in malignant tumours and promotes the proliferation and invasion of tumour cells through the activation of the NF-κB signalling pathway (42). Second mitochondria-derived activator of caspases (SMAC) is an endogenous antagonist of cIAP1, cAIP2 and XIAP and promotes apoptosis by binding IAPs and preventing the inhibition of caspases 3, 7 and 9 (43).…”

Section: Discussionmentioning

confidence: 99%

DPP3 expression promotes cell proliferation and migration in vitro and tumour growth in vivo, which is associated with poor prognosis of oesophageal carcinoma

et al. 2022

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Dipeptidyl peptidase III (DPP3), a zinc-dependent metallopeptidase, is upregulated in a variety of malignancies. However, little is known about its roles in the pathogenesis of these malignancies. The present study was designed to investigate the roles of DPP3 in the pathogenesis and progression of oesophageal cancer (EC). The expression level of DPP3 in EC tissues and adjacent normal tissues was detected in 93 cases of tissue biopsies collected from patients diagnosed with oesophageal carcinoma by immunohistochemistry. The effect of DPP3 expression on cell proliferation, migration or apoptosis was determined in DPP3-depleted EC cells created by infection with lentivirus containing short hairpin RNA specific to the human DPP3 mRNA sequence, followed by detection at the cellular level using a Celigo cell count assay, flow cytometry, wound-healing assay and Transwell assay as well as chip screening with a Human Apoptosis Antibody Array kit, which enables the quantitative detection of 43 apoptosis-related genes. A xenograft model was applied to detect the tumour growth and invasion of DPP3-depleted cancer cells in nude mice. The results revealed that DPP3 expression was elevated in EC tissues compared with adjacent non-tumour tissues, and high DPP3 expression was significantly associated with poor prognosis. DPP3 depletion resulted in reduced cell proliferation and migration and enhanced cell cycle arrest and apoptosis of EC cells and led to the inhibition of tumour growth and invasion in a xenograft model. In addition, DPP3 depletion was associated with the upregulation of the proapoptotic proteins SMAC and p53 and the downregulation of the antiapoptotic proteins clAP-2, IGFBP-2 and TRAILR-4. Finally, DPP3 may promote cell proliferation, migration and survival of EC cells in vitro and tumour growth and invasion of oesophageal carcinoma in vivo, and thus may serve as a molecular target for tumour therapy.

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Section: Discussionmentioning

confidence: 99%

DPP3 expression promotes cell proliferation and migration in vitro and tumour growth in vivo, which is associated with poor prognosis of oesophageal carcinoma

et al. 2022

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“…CIAP2, encoded by BIRC3, is one of the eight human inhibitors of apoptosis proteins (IAPs) that contribute to apoptosis escape of cancer cells [ 54 , 55 ]. CIAP2 has become an exciting research topic because of its exceedingly elevated expression in a wide range of cancers, including gallbladder cancer [ 27 ], gastric cancer [ 56 ], renal cell carcinomas [ 57 ], and, unsurprisingly, HCC [ 28 ]. Mechanistically, cIAP2 and cIAP1 are both E3 ubiquitin ligases.…”

Section: Discussionmentioning

confidence: 99%

CircNUP54 promotes hepatocellular carcinoma progression via facilitating HuR cytoplasmic export and stabilizing BIRC3 mRNA

Tang,

Zhuang,

Wang

et al. 2024

Cell Death Dis

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Circular RNAs (circRNAs) have been implicated in tumorigenesis and progression of various cancers. However, the underlying mechanisms of circRNAs in hepatocellular carcinoma (HCC) have not been fully elucidated. Herein, a new oncogenic circRNA, hsa_circ_0070039 (circNUP54), was identified to be significantly upregulated in HCC through circRNA sequencing. As verified in 68 HCC samples, circNUP54 overexpression was correlated with aggressive cancerous behaviors and poor outcomes. Moreover, the function experiments showed that knockdown of circNUP54 inhibited the malignant progression of HCC in vitro and in vivo, whereas overexpression of circNUP54 had the opposite role. Mechanistic investigations carried out by RNA pull-down, RNA immunoprecipitation, and immunofluorescence revealed that circNUP54 interacted with the RNA-binding protein Hu-antigen R (HuR) and promoted its cytoplasmic export. The cytoplasmic accumulation of HuR stabilized the downstream BIRC3 mRNA through its binding to the 3′ UTR region. Consequently, the encoded protein of BIRC3, cellular inhibitor of apoptosis 2 (cIAP2), proceeded to activate the NF-κB signal pathway and ultimately contributed to HCC progression. In addition, depletion of BIRC3 rescued the pro-tumorigenic effect of circNUP54 on HCC cells. Overall, this study demonstrated that circNUP54 facilitates HCC progression via regulating the HuR/BIRC3/NF-κB axis, which may serve as a promising therapeutic target for HCC treatment.

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“…Cellular inhibitor of apoptosis (cIAP2) plays a role in degrading caspases by linking them to ubiquitin molecules and supports cell survival by preventing cellular apoptosis of cancer cells [46][47][48]. cIAP-2 is upregulated in malignant tumors, and promotes proliferation and invasion of tumor cells through the activation of NF-κB signaling pathway [49][50]. Second mitochondria-derived activator of caspases (SMAC) is an endogenous antagonist of cIAP1, cAIP2 and XIAP, and promotes apoptosis by binding IAPs and preventing the inhibition of caspases 3, 7, and 9 [51].…”

Section: Discussionmentioning

confidence: 99%

DPP3 Expression Promotes Cell Proliferation and Migration in Vitro and Tumor Growth in Vivo That Associates with Poor Prognosis of Esophageal Carcinoma

Liu

Abudula

Yang

et al. 2021

Preprint

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Background: Dipeptidyl peptidase III (DPP3) is a zinc-dependent metallopeptidase and elevated in a variety of malignant tumors, but the underlying mechanism is not well understood so far. Here we investigated the association of esophageal carcinogenesis with the regulation of DPP3 expression by tissue-based quantitative analysis and the depletion of DPP3 expression in esophageal cancer cells and xenograft model. Methods: The expression level of DPP3 in esophageal cancer tissues and adjacent normal tissues was detected in 93 cases of tissue biopsies collected from patients diagnosed with esophageal carcinoma by immunohistochemistry. The effect of DPP3 expression on cell proliferation, migration or apoptosis was determined in DPP3-depleted esophageal cancer cells created by infection with the lentivirus containing the shRNA specific to human DPP3 mRNA sequence followed by cytometric detection using celigo cell count assay, flow cytometry, wound-healing assay and trans-well assay as well as chip screening with a Human Apoptosis Antibody Array kit, which enables the quantitative detection of 43 apoptosis-related genes. A xenograft model was applied to the detection of tumor growth and invasion of DPP3-depleted cancer cells in nude mice.Results: DPP3 expression was elevated in esophageal cancer tissues compared with adjacent non-tumor tissues (normal controls) with statistical significance (P<0.05), and associated with poor prognosis of esophageal carcinoma. The DPP3-depletion resulted in a reduced cell proliferation and migration and enhanced cell-cycle arrest and apoptosis of esophageal cancer cells, and lead to the inhibition of tumor growth and invasion in xenograft model. In addition, DPP3-depletion was associated with the upregulation of pro-apoptotic proteins and the downregulation of anti-apoptotic proteins.Conclusions: These findings suggest that DPP3 may promote cell proliferation, migration and survival of esophageal cancer cells in vitro, and tumor growth and invasion of esophageal carcinoma in vivo and this might serve as a molecular target for tumor therapy.

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cIAP2 via NF-κB signalling affects cell proliferation and invasion in hepatocellular carcinoma

Cited by 12 publications

References 41 publications

DPP3 expression promotes cell proliferation and migration in vitro and tumour growth in vivo, which is associated with poor prognosis of oesophageal carcinoma

DPP3 expression promotes cell proliferation and migration in vitro and tumour growth in vivo, which is associated with poor prognosis of oesophageal carcinoma

CircNUP54 promotes hepatocellular carcinoma progression via facilitating HuR cytoplasmic export and stabilizing BIRC3 mRNA

DPP3 Expression Promotes Cell Proliferation and Migration in Vitro and Tumor Growth in Vivo That Associates with Poor Prognosis of Esophageal Carcinoma

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