Autophagy and apoptosis in liver injury

Wang, Kewei

doi:10.1080/15384101.2015.1038685

Cited by 300 publications

(218 citation statements)

References 138 publications

(167 reference statements)

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“…Despite the progress achieved in understanding the cancer process and the impact of this knowledge on treatment, primary prevention remains the most effective approach to reduce cancer mortality in both developed and developing countries for the near future [9,37,38,50,51,56,309] . …”

Section: Future Directionsmentioning

confidence: 99%

Hepatocellular carcinoma and the risk of occupational exposure

Rapisarda

Loreto

Malaguarnera

et al. 2016

WJH

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Hepatocellular carcinoma (HCC) is the most common type of liver cancer. The main risk factors for HCC are alcoholism, hepatitis B virus, hepatitis C virus, nonalcoholic steatohepatitis, obesity, type 2 diabetes, cirrhosis, aflatoxin, hemochromatosis, Wilson's disease and hemophilia. Occupational exposure to chemicals is another risk factor for HCC. Often the relationship between occupational risk and HCC is unclear and the reports are fragmented and inconsistent. This review aims to summarize the current knowledge regarding the association of infective and non-infective occupational risk exposure and HCC in order to encourage further research and draw attention to this global occupational public health problem. Core tip: Hepatocellular carcinoma (HCC) is the fifth most common human cancer. This review summarizes current knowledge regarding the occupational risk factors of HCC. In particular, we underline not only the infective but also non-infective occupational risk exposure, including chemical agents and toxic metabolites which are a major cause of liver damage.

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Section: Future Directionsmentioning

confidence: 99%

Hepatocellular carcinoma and the risk of occupational exposure

Rapisarda

Loreto

Malaguarnera

et al. 2016

WJH

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“…Another important factor for autophagosome formation is Beclin-1, a 60-kDa protein encoded by the Beclin-1 gene. This protein regulates autophagosome formation through binding to class III PI3K [7] . In this study, RT-PCR and Western blot results showed that BMA-155Cl increased the expression of Beclin-1 and LC3B and the amount of LC3B that accumulated in the presence of pepstatin A, indicating the occurrence of autophagy induced by BMA-155Cl in HepG-2 cells.…”

Section: Discussionmentioning

confidence: 99%

“…The cross-talk between apoptosis and autophagy is critical to cell fate but is complicated by the contradictory roles of apoptosis and autophagy under some conditions. Autophagy and apoptosis synergistically affect each other [7] . Hepatocellular carcinoma (HCC) is a common primary tumor [9,10] .…”

Section: Original Articlementioning

confidence: 99%

“…The complex interplay between hepatic autophagy and apoptosis determines the degree of hepatic apoptosis and the progression of liver disease. The autophagic pathway may be a novel therapeutic target for liver disease [7] . Therefore, scholars must screen and develop chemical compounds that can effectively inhibit HCC through the autophagic pathway to benefit public health.…”

Section: Original Articlementioning

confidence: 99%

“…However, autophagic cells coping with excessive stress may commit suicide by undergoing autophagic cell death [4] . Autophagy plays an important role in the regulation of cell survival and cell death, especially in apoptosis-signaling pathways [7] . Considerable cross-talk exists between autophagy and apoptosis.…”

Section: Introductionmentioning

confidence: 99%

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Bisindolylmaleimide alkaloid BMA-155Cl induces autophagy and apoptosis in human hepatocarcinoma HepG-2 cells through the NF-κB p65 pathway

Sun

et al. 2017

Acta Pharmacol Sin

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Bisindolylmaleimides, a series of derivatives of a PKC inhibitor staurosporine, exhibit potential as anti-cancer drugs and have received considerable attention in clinical trials. This study aims to investigate the effects of a bisindolylmaleimide alkaloid 155Cl (BMA-155Cl) with a novel structure on autophagy and apoptosis in human hepatocarcinoma HepG-2 cells in vitro and in vivo. The cell poliferation was assessed with a MTT assay. Autophagy was evaluated by MDC staining and TEM analysis. Apoptosis was investigated using Annexin V-FITC/PI and DAPI staining. The antitumor effects were further evaluated in nude mice bearing HepG-2 xenografts, which received BMA-155Cl (10, 20 mg/kg, ip) for 18 days. Autophagy-and apoptosis-associated proteins and their mRNA levels were examined with Western blotting, immunohistochemistry, and RT-PCR. BMA-155Cl (2.5-20 μmol/L) inhibited the growth of HepG-2 cells with IC 50 values of 16.62±1.34, 12.21±0.83, and 8.44±1.82 μmol/L at 24, 48, and 72 h, respectively. Furthermore, BMA155Cl (5-20 μmol/L) dose-dependently induced autophagy and apoptosis in HepG-2 cells. The formation of autophagic vacuoles was induced by BMA-155Cl (10 μmol/L) at approximately 6 h and peaked at approximately 15 h. Pretreatment with 3-MA potentiated BMA-155Cl-mediated apoptotic cell death. This compound dose-dependently increased the mRNA and protein levels of Beclin-1, NF-κB p65, p53, and Bax, but decreased the expression of IκB and Bcl-2. Pretreatment with BAY 11-7082, a specific inhibitor of NF-κB p65, blocked BMA-155Cl-induced expression of autophagy-and apoptosis-associated proteins. BMA-155Cl administration effectively suppressed the growth of HepG-2 xenografts in vivo, and increased the protein expression levels of LC3B, Beclin-1, NF-κB p65, and Bax in vivo. We conclude that the NF-κB p65 pathway is involved in BMA-155Cl-triggered autophagy, followed by apoptosis in HepG-2 cells in vitro and in vivo. Hence, BMA-155Cl could be a promising pro-apoptotic candidate for developing as a novel anti-cancer drug.

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RETRACTED: Combination of aloin and metformin enhances the antitumor effect by inhibiting the growth and invasion and inducing apoptosis and autophagy in hepatocellular carcinoma through PI3K/AKT/mTOR pathway

Sun

Zhai²,

et al. 2019

Cancer Medicine

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Hepatocellular carcinoma (HCC) is a devastating and highly metastatic cancer worldwide. Metformin (MET) is the priority drug for treatment of type 2 diabetes; however, it possesses multiple biological effects like anticancer and hepatoprotective activity. Herein, we examined the effects of aloin (barbaloin) and MET as well as combination treatment in HCC cell line in vitro and in vivo. As a result, aloin and MET alone exhibited inhibitory effects on proliferation and invasion of HepG2 and Bel‐7402 cells. Specially, combination treatment of aloin and MET showed enhanced inhibitory effects in vitro. Aloin and MET alone induced apoptosis and autophagy in vitro. Similarly, aloin and MET cooperated to promote apoptosis and autophagy in HepG2 and Bel‐7402 cells. In the HepG2 xenograft models, aloin in combination with MET confine tumor growth and facilitate apoptosis and autophagy. Both the in vitro and in vivo results showed that aloin and MET alone as well as combination treatment activated the PI3K/AKT/mTOR pathway. Overall, our research demonstrated that the concomitant treatment with aloin and MET enhances the antitumor effect by inhibiting the growth and invasion as well as inducing apoptosis and autophagy in HCC through PI3K/AKT/mTOR pathway.

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Autophagy and apoptosis in liver injury

Cited by 300 publications

References 138 publications

Hepatocellular carcinoma and the risk of occupational exposure

Hepatocellular carcinoma and the risk of occupational exposure

Bisindolylmaleimide alkaloid BMA-155Cl induces autophagy and apoptosis in human hepatocarcinoma HepG-2 cells through the NF-κB p65 pathway

RETRACTED: Combination of aloin and metformin enhances the antitumor effect by inhibiting the growth and invasion and inducing apoptosis and autophagy in hepatocellular carcinoma through PI3K/AKT/mTOR pathway

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