XPD Functions as a Tumor Suppressor and Dysregulates Autophagy in Cultured HepG2 Cells

Zhang, Jixiang

doi:10.12659/msm.894303

Cited by 8 publications

(6 citation statements)

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“…With specific respect to HCC, recent studies have tied XPD to increased HCC susceptibility [20, 21]. XPD expression serves as a tumor suppressor in HCC [22]. To better understand XPD’s role in HCC, we investigated the in vitro cellular effects of XPD expression in HCC cells through transfection of the XPD gene into the HCC cell line SMMC7721 and Hep3B.…”

Section: Discussionmentioning

confidence: 99%

XPD suppresses cell proliferation and migration via miR-29a-3p-Mdm2/PDGF-B axis in HCC

2019

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ObjectiveThe aim of this study was to investigate the role of XPD in migration and invasion of hepatocellular carcinoma (HCC) cells.MethodsThe expression of XPD and miR-29a-3p was examined by western blot and qRT-PCR, cell proliferation was detected by MTT assay, cell migration was detected by transwell assay. TargetScan was used to predict potential targets of miR-29a-3p.ResultsIn this study, we found that the expression of XPD and miR-29a-3p was downregulated in HCC samples and HCC cell lines. XPD suppressed proliferation and migration of HCC cell via regulating miR-29a-3p expression. Target prediction analysis and dual-luciferase reporter assay confirmed Mdm2 and PDGF-B were direct targets of miR-29a-3p, and miR-29a-3p suppressed proliferation and migration of HCC cells via regulating the expression of Mdm2 or PDGF-B.ConclusionsOur data indicated that XPD suppressed cell proliferation and migration via miR-29a-3p-Mdm2/PDGF-B axis in HCC.

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Section: Discussionmentioning

confidence: 99%

XPD suppresses cell proliferation and migration via miR-29a-3p-Mdm2/PDGF-B axis in HCC

2019

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“…Autophagy is characterized by the presence of a large number of autophagosomes in the cytoplasm, and various digestive enzymes in the lysosome digest and degrade the contents in the vacuoles to convert them into substances required by the body for energy ( 32 , 33 ). Several studies have confirmed that autophagy plays an important role in tumorigenesis and therapy ( 34 – 36 ). However, reports on the effect of autophagy induced by drugs in tumor cells are not consistent and suggest that autophagy can have synergistic or antagonistic effects with apoptosis ( 37 , 38 ).…”

Section: Introductionmentioning

confidence: 98%

Reduction of apoptosis by proanthocyanidin-induced autophagy in the human gastric cancer cell line MGC-803

Nie

Zhou

Qin³

et al. 2015

Oncology Reports

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Proanthocyanidins are flavonoids that are widely present in the skin and seeds of various plants, with the highest content in grape seeds. Many experiments have shown that proanthocyanidins have antitumor activity both in vivo and in vitro. Autophagy and apoptosis of tumor cells induced by drugs are two of the major causes of tumor cell death. However, reports on the effect of autophagy induced by drugs in tumor cells are not consistent and suggest that autophagy can have synergistic or antagonistic effects with apoptosis. This research was aimed at investigating whether proanthocyanidins induced autophagy and apoptosis in human gastric cancer cell line MGC-803 cells and to identify the mechanism of proanthocyanidins action to further determine the effect of proanthocyanidins-induced autophagy on apoptosis. MTT assay was used to examine the proanthocyanidin cytotoxicity against human gastric cancer cell line MGC-803. Transmission electron microscopy and monodansylcadaverine (MDC) staining were used to detect autophagy. Annexin V APC/7-AAD double staining and Hoechst 33342/propidium iodide (PI) double staining were used to explore apoptosis. Western blotting was used to determine expression of proteins related to autophagy and apoptosis. Real-time quantitative PCR technology was used to determine the mRNA level of Beclin1 and BCL-2. The results showed that proanthocyanidins exhibit a significant inhibitory effect on the human gastric cancer cell line MGC-803 proliferation in vitro and simultaneously activate autophagy and apoptosis to promote cell death. Furthermore, when proanthocyanidin-induced autophagy is inhibited, apoptosis increases significantly, proanthocyanidins can be used together with autophagy inhibitors to enhance cytotoxicity.

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“…XPD751 polymorphism has been shown to be associated with the occurrence and development of a wide range of malignancies, such as esophageal cancer, gastric cancer, and colorectal cancer (26)(27)(28). Previous studies have demonstrated that XPd expression serves as a tumor suppressor in Hcc (10,11,29). In a present study by the authors, it was found that the mRNA and protein expression levels of XPD in ESCC tissue samples were significantly lower than those in the adjacent normal esophageal tissue samples.…”

Section: Discussionmentioning

confidence: 40%

XPD inhibits cell growth and invasion and enhances chemosensitivity in esophageal squamous cell carcinoma by regulating the PI3K/AKT signaling pathway

Jian

Liu

et al. 2020

Int J Mol Med

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Esophageal squamous cell carcinoma (EScc) is a lethal disease due to its high aggressiveness. The aim of the present study was to investigate the role of xeroderma pigmentosum complementation group d (XPd) in the growth and invasion of EScc and to elucidate the potential underlying molecular mechanisms. Western blot analysis and RT-qPcR were used to detect the expression level of XPd in EScc tissue samples and adjacent normal esophageal tissue samples. The pEGFP-N2/XPd plasmid was transfected into human EScc cell lines (Ec9706 and Ec109). The proliferation, apoptosis, migration and invasion of Ec9706 or Ec109 cells were assessed following transfection with the XPd overexpression plasmid. The chemosensitivity of Ec9706 or Ec109 cells to cisplatin or fluorouracil was evaluated by CCK-8 assay. The expression levels of phosphoinositide 3-kinase (PI3K)/AKT, nuclear factor (NF)-κB, Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) and mitogen-activated protein kinase (MAPK) signaling pathway-related genes were detected by RT-qPcR and western blot analysis. The results demonstrated that the expression level of XPd was markedly lower in EScc tissue samples than in adjacent normal esophageal tissue samples. The pEGFP-N2/XPd plasmid was successfully transfected into Ec9706 or Ec109 cells, inducing XPd overexpression. A High XPd expression markedly suppressed cell proliferation, migration and invasion, and increased the apoptotic rate of Ec9706 and Ec109 cells. Furthermore, the overexpression of XPD significantly increased the chemosensitivity of Ec9706 and Ec109 cells to cisplatin or fluorouracil. Following XPD overexpression, the expression levels of PI3K, p-AKT, c-Myc, Cyclin D1, Bcl-2, vascular endothelial growth factor (VEGF) and matrix metalloproteinase (MMP)-9 were markedly downregulated, while the expression level of p21 was markedly upregulated. On the whole, the findings of the present study demonstrate that XPd inhibits the growth and invasion of Ec9706 and Ec109 cells, whilst also enhancing the chemosensitivity of Ec9706 and EC109 cells to cisplatin or fluorouracil by regulating the PI3K/AKT signaling pathway. XPD may thus be an underlying target for EScc treatment and drug resistance.

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XPD Functions as a Tumor Suppressor and Dysregulates Autophagy in Cultured HepG2 Cells

Cited by 8 publications

References 23 publications

XPD suppresses cell proliferation and migration via miR-29a-3p-Mdm2/PDGF-B axis in HCC

XPD suppresses cell proliferation and migration via miR-29a-3p-Mdm2/PDGF-B axis in HCC

Reduction of apoptosis by proanthocyanidin-induced autophagy in the human gastric cancer cell line MGC-803

XPD inhibits cell growth and invasion and enhances chemosensitivity in esophageal squamous cell carcinoma by regulating the PI3K/AKT signaling pathway

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