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Background: Hepatocellular carcinoma (HCC) with tumor thrombus in the bile duct (BDTT) is easily misdiagnosed or mistreated due to the clinicopathological diversity of the thrombus and its relationship with primary lesions., Aim: To propose a new classification for HCC with BDTT in order to guide its diagnosis and treatment., Methods: A retrospective review of the diagnosis and treatment experience regarding seven typical HCC patients with BDTT between January 2010 and December 2019 was conducted., Results: BDTT was preoperatively confirmed by computed tomography/magnetic resonance imaging in only four patients. Three patients with recurrent HCC and one patient with first-occurring HCC had no visible intrahepatic tumors; of these, misdiagnosis occurred in two patients, and three patients died. One patient was mistreated as having common bile duct stones, and another patient with a history of multiple recurrent HCC was misdiagnosed until obvious biliary dilation could be detected. Only one patient who received hepatectomy accompanied by BDTT extraction exhibited disease-free survival during the follow-up period. A new classification was proposed for HCC with BDTT as follows: HCC with microscopic BDTT (Type I); resectable primary or recurrent HCC mass in the liver with BDTT (Type II); BDTT without an obvious HCC mass in the liver (Type III) and BDTT accompanied with unresectable intra- or extrahepatic HCC lesions (Type IV)., Conclusion: We herein propose a new classification system for HCC with BDTT to reflect its pathological characteristics and emphasize the significance of primary tumor resectability in its treatment., Competing Interests: Conflict-of-interest statement: We have no financial relationships to disclose., (©The Author(s) 2020. Published by Baishideng Publishing Group Inc. All rights reserved.)

Objective: The aim of this study was to investigate long non-coding RNA (lncRNA) TP73-AS1 expression in hepatocellular carcinoma (HCC) tissues and cells, and to further investigate whether it can accelerate the progression of HCC by regulating microRNA-103., Patients and Methods: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to examine TP73-AS1 expression in 60 pairs of HCC tissues and adjacent ones, and the association between lncRNATP73-AS1 level and clinical indicators of HCC as well as patients' prognosis was analyzed. Meanwhile, qRT-PCR was used to further verify TP73-AS1 expression in HCC cell lines. The lncRNA TP73-AS1 knockdown model was constructed using lentivirus in the HCC cell lines, including Bel-7402 and HepG2. Cell counting kit-8 (CCK-8), 5-Ethynyl-2'-deoxyuridine (EdU), and flow cytometry assays were performed to figure out the influence of TP73-AS1 on the basic biological function of the HCC cells. Finally, the involved potential regulatory mechanism was explored using cell recovery experiments, and the relationship between TP73-AS1 and microRNA-103 was further studied., Results: QRT-PCR results indicated that TP73-AS1 expression in HCC samples was conspicuously enhanced compared with paracancerous tissues, and patients with a relatively high level of TP73-AS1 had a higher tumor stage and a lower overall survival rate. Meanwhile, the proliferation ability of cells in the sh-TP73-AS1 group was strikingly lower than that in the control group, while cell apoptosis showed the opposite trend. Besides, qRT-PCR results indicated a negative correlation between microRNA-103 and TP73-AS1 in HCC tissue specimens. The results of the luciferase reporting assay revealed that TP73-AS1 could be targeted by microRNA-103 through binding site. In addition, the cell recovery experiment demonstrated that TP73-AS1 and microRNA-103 might have a mutual regulation, and the two of which could together affect the malignant progression of HCC., Conclusions: TP73-AS1 expression was conspicuously enhanced both in HCC tissues and cell lines, which were associated with advanced tumor stage and poor prognosis. In addition, TP73-AS1 could accelerate the proliferation of HCC cells by regulating microRNA-103.

Multidrug resistance (MDR) is one of the major reasons for the failure of liver cancer chemotherapy, and its suppression may increase the efficacy of chemotherapy. NANOG plays a key role in the regulation of embryonic stem cell self-renewal and pluripotency. Recent studies reported that NANOG was abnormally expressed in several types of tumors, indicating that NANOG is related to tumor development. However, the correlation between NANOG and liver cancer chemoresistance remains uncertain. In this study, RNA interfere technology was employed to knock down NANOG expression in HepG2 human liver cancer cells. We found that the knockdown of NANOG expression in NANOG siRNA-transfected HepG2 cells resulted in decreased colony formation rate and cell migration compared to control HepG2 cells. In addition, HepG2 cells were treated with doxorubicin to evaluate the chemosensitivity to doxorubicin. We found that the doxorubicin sensitivity of HepG2 cells was increased with downregulation of NANOG expression. The expression of MDR1 at both mRNA and protein levels was decreased in HepG2 cells when NANOG was knocked down. These findings suggest that the knockdown of NANOG in HepG2 human cells resulted in decreased MDR1 expression and increased doxorubicin sensitivity, and NANOG could be used as a novel potential therapeutic target to reverse multidrug resistance of liver cancer.