Hepatocellular carcinoma (Hcc) is one of the primary causes of cancer-associated deaths worldwide. current treatment methods include surgical resection, chemotherapy and radiotherapy; however the curative rate remains low, thus novel treatments are required. The aim of the present study was to investigate the role of targeting protein for Xenopus kinesin-like protein 2 (TPX2) in the growth of Hcc and its underlying molecular mechanism. Immunohistochemistry staining, reverse transcription-quantitative (RT-q)PcR and western blotting were used to detect the expression of TPX2 mRNA and protein in liver cancer tissue samples, adjacent normal liver tissue samples, and the Hcc cell lines Huh7, Hep3B, PLc/PRF/5 and MHcc97-H. The recombinant plasmid pMagic4.1-shRNA-TPX2 was constructed and transfected into Huh7 and Hep3B Hcc cells to silence TPX2 expression. The proliferation, apoptosis, migration and invasion of Huh7 cells and Hep3B cells were evaluated before and after TPX2 silencing. The mRNA and protein expression levels of multiple signaling pathway-associated genes were detected by RT-qPcR and western blotting. The expression levels of TPX2 mRNA and protein were significantly higher in Hcc tissue samples compared with adjacent normal liver tissue sample. TPX2 mRNA and protein expression levels were detected in the different Hcc cell lines. The recombinant plasmid pMagic4.1-shRNA-TPX2 was successfully transfected into Huh7 and Hep3B cells, resulting in TPX2 silencing. TPX2 knockdown significantly reduced cell proliferation, cell migration and cell invasion of Huh7 and Hep3B cells, whilst also increasing the rate of apoptosis in these cells. Following TPX2 silencing, the expression levels of PI3K, phospho-AKT, Bcl-2, c-Myc and Cyclin D1 were significantly decreased, whereas the expression levels of P21 and P27 were significantly increased. In conclusion, TPX2 may suppress the growth of Hcc by regulating the PI3K/AKT signaling pathway and thus, TPX2 may be a potential target for the treatment of liver cancer.

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.