Hepatocellular carcinoma (HCC): beyond sorafenib—chemotherapy

Kim, Dae Won; Talati, Chetasi; Kim, Richard

doi:10.21037/jgo.2016.09.07

Cited by 255 publications

(181 citation statements)

References 68 publications

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“…It is estimated that the incidence of HCC and HCC-related deaths have increased over the last several decades in many parts of the world [2]. The strongest risk factors for HCC are chronic hepatitis B virus (HBV) and/or hepatitis C virus (HCV) infections, which account for the vast majority of primary HCCs [3].…”

Section: Introductionmentioning

confidence: 99%

Long Noncoding RNA HOST2 Promotes Epithelial-Mesenchymal Transition, Proliferation, Invasion and Migration of Hepatocellular Carcinoma Cells by Activating the JAK2-STAT3 Signaling Pathway

Tan

Wang

et al. 2018

Cell Physiol Biochem

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Background/Aims: This study aims to examine the effect of long noncoding RNA HOST2 (LncRNA HOST2) on epithelial-mesenchymal transition (EMT), proliferation, invasion and migration of hepatocellular carcinoma (HCC) cells via activation of the JAK2-STAT3 signaling pathway. Methods: HCC and para-cancerous tissues were collected from 136 HCC patients. Immunohistochemistry was used to detect the expression of JAK2 and STAT3. HCC SMMC7721 cells were grouped into blank, negative control (NC), HOST2 mimic and HOST2 inhibitor groups. The mRNA and protein expression levels of HOST2, JAK2, STAT3, E-cadherin, vimentin, Snail, Slug, Twist and Zeb1 in tissues and cells were determined by reverse transcription -quantitative polymerase chain reaction (RT-qPCR) and Western blotting, respectively. An MTT assay, scratch test and Transwell assay were applied to measure cell proliferation, migration and invasion, respectively. Results: The levels of JAK2, STAT3 and vimentin were higher in HCC tissues, while the expression of E-cadherin was lower in HCC tissues compared with para-cancerous tissues. The silencing of HOST2 significantly decreased cell proliferation, migration and invasion, reduced the levels of HOST2, JAK2, STAT3 and vimentin, and elevated the expression of E-cadherin. HOST2 silencing also decreased the levels of Snail, Slug and Twist but increased the level of Zeb1 protein, while the opposite findings were observed in the HOST2 mimic group. Conclusion: These results reveal a possible mechanism in HCC in which LncRNA HOST2 may increase EMT and enhance proliferation, invasion and metastasis of HCC cells via activation of the JAK2-STAT3 signaling pathway.

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Section: Introductionmentioning

confidence: 99%

Long Noncoding RNA HOST2 Promotes Epithelial-Mesenchymal Transition, Proliferation, Invasion and Migration of Hepatocellular Carcinoma Cells by Activating the JAK2-STAT3 Signaling Pathway

Tan

Wang

et al. 2018

Cell Physiol Biochem

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“…Liver cancer, one principal cause of cancer‐related death globally, is associated with a relatively high incidence of 850 000 new cases annually, and hepatocellular carcinoma (HCC) accounts for up to 90% of the primary liver cancer . Although there exits diverse treatments for HCC (eg, surgical resection, liver transplantation, transarterial chemoembolization, radical therapy, and systemic therapy), the late‐stage diagnoses, and the increased drug‐/radiation‐resistant degree made it tough to cure the disorder . Specifically, while chemotherapeutics and radioactive rays induced cell apoptosis, certain anti‐apoptotic factors synthesized by the carcinoma cells (eg, Livin) would induce apoptotic resistance, which could, to a great extent, explain the drug resistance of cancers .…”

Section: Introductionmentioning

confidence: 99%

The LncRNA H19/miR‐193a‐3p axis modifies the radio‐resistance and chemotherapeutic tolerance of hepatocellular carcinoma cells by targeting PSEN1

Liu

et al. 2018

J of Cellular Biochemistry

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This study was designated to verify if the lncRNA H19/miR-193a-3p axis would play a regulatory role in the radio-/chemo-resistances of HCC cells through targeting PSEN1. Within the study, five human HCC cell lines were prepared, including Bel-7402, HepG2, Hep3b, QGY-7703, and SMMC-7721. Moreover, docetaxel (DT), paclitaxel (Pt), vinorelbine (Vb), and 5-fluorouracil (5-Fu) were managed as the chemo-therapeutics, and single-dose X-rays were performed as radio-therapies. Besides, lncRNA H19 and miR-193a-3p were detected by qRT-PCR and Western blot were implemented to quantify the expressional levels of PSEN1, Ku80, γ-H2AX, and RAD51. Luciferase reporter gene assay was advanced to verify the targeted relationship between lncRNA H19 and miR-193a-3p. As a consequence, QGY-7703 and Bel-7402 were, respectively, the most radiation-sensitive and radiation-proof cell lines, and Bel-7402 was associated with the highest resistances to DT, Pt, Vb, and 5-FU. The restrained lncRNA H19 and over-expressed miR-193a-3p expressions tended to significantly elevate the survival rate and proliferation of Bel-7402 cells, when they were exposed to radiation and subject to chemo-therapies. The lncRNA H19 was also found to directly target miR-193a-3p in inducing the HCC development. PSEN1 appeared to be subject to the modification of lncRNA H19 and miR-193a-3p in its acting on the survival rates and proliferative abilities of HCC cells. The lncRNA H19/miR-193a-3p/PSEN1 axis could be regarded as the treatment targets for HCC, so as to further improve the treatment efficacy of chemo- and radio-therapies for HCC.

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“…Chemoresistance is a major cause of treatment failure and is an important challenge for cancer therapy (Kim et al, 2017). Therefore, identifying the molecular markers of chemoresistance and increasing tumor-cell sensitivity to chemotherapeutic drugs are critical for enhancing therapeutic efficacy.…”

Section: Discussionmentioning

confidence: 99%

Lin28B is involved in curcumin-reversed paclitaxel chemoresistance and associated with poor prognosis in hepatocellular carcinoma

Tian

Shangguan

Zhou

et al. 2018

Preprint

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statement upregulation of Lin28B not only confers poor prognosis in HCC patients but also increases chemoresistance in HCC cells. Thus, Lin28B may serve as a predictive biomarker for use to reverse chemoresistance in clinical practice. AbstractChemoresistance remains a big challenge in hepatocellular carcinoma (HCC) treatment. Several studies indicated that RNA-binding protein Lin28B serves an oncogenic role in HCC, but its activity in HCC chemotherapy has never been assessed. In this study, we found that overexpression of Lin28B significantly increased the paclitaxel chemoresistance in two different HCC cells lines while silencing Lin28B reduced the chemoresistance in paclitaxel-resistance HCC cells. Curcumin, a natural anti-cancer agent, increased the sensitivity of HCC cells to paclitaxel through inhibiting NF-κB stimulated Lin28B expression both in vitro and in vivo. Furthermore, by analyzing TCGA (The Cancer Genome Atlas) LIHC (liver hepatocellular carcinoma) and GSE14520 databases, we found that Lin28B was highly up-regulated in HCC tissue compared with that in normal tissue and associated with -fetoprotein levels, and that patients with Lin28B higher expression had a significant shorter overall survival time than those with Lin28B lower expression. Our data reveal that Lin28B may serve as a predictive biomarker and a treatment target to reverse HCC chemotherapy resistance in future clinical practice.

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Hepatocellular carcinoma (HCC): beyond sorafenib—chemotherapy

Cited by 255 publications

References 68 publications

Long Noncoding RNA HOST2 Promotes Epithelial-Mesenchymal Transition, Proliferation, Invasion and Migration of Hepatocellular Carcinoma Cells by Activating the JAK2-STAT3 Signaling Pathway

Long Noncoding RNA HOST2 Promotes Epithelial-Mesenchymal Transition, Proliferation, Invasion and Migration of Hepatocellular Carcinoma Cells by Activating the JAK2-STAT3 Signaling Pathway

The LncRNA H19/miR‐193a‐3p axis modifies the radio‐resistance and chemotherapeutic tolerance of hepatocellular carcinoma cells by targeting PSEN1

Lin28B is involved in curcumin-reversed paclitaxel chemoresistance and associated with poor prognosis in hepatocellular carcinoma

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