Transactivation of proto-oncogene c-Myc by hepatitis B virus transactivator MHBst167

Lun, Yongzhi; Cheng, Jun; Chi, Qing; Wang, Xue‐Lei; Gao, Meng; Sun, Liping

doi:10.3892/ol.2014.2190

Cited by 2 publications

(3 citation statements)

References 16 publications

(13 reference statements)

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“…Telomerase activation is observed in over 90% of HCC patients and is closely related to HCC 177 . C‐terminally truncated middle surface protein of hepatitis B virus (MHBst) and wild‐type/truncated HBx proteins activate the transcripts promoter of TERT in HBV‐associated HCC 178 . Many signaling pathways were activated in HCC such as Wnt/β‐Catenin, cell cycle, oxidative stress metabolic pathway, Ras/ MAPK, and so on 179 …”

Section: Human Carcinogenic or Cancer‐promoting Microbiomesmentioning

confidence: 99%

“…177 C-terminally truncated middle surface protein of hepatitis B virus (MHBst) and wild-type/truncated HBx proteins activate the transcripts promoter of TERT in HBVassociated HCC. 178 Many signaling pathways were activated in HCC such as Wnt/β-Catenin, cell cycle, oxidative stress metabolic pathway, Ras/ MAPK, and so on. 179 Whether HCV can induce HCC is unknown, but it is a primary risk factor for the disease.…”

Section: 81mentioning

confidence: 99%

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Human microbiomes in cancer development and therapy

Xia

Liu

et al. 2023

MedComm

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Colonies formed by bacteria, archaea, fungi, and viral groups and their genomes, metabolites, and expressed proteins constitute complex human microbiomes. An increasing evidences showed that carcinogenesis and disease progression were link to microbiomes. Different organ sources, their microbial species, and their metabolites are different; the mechanisms of carcinogenic or procancerous are also different. Here, we summarize how microbiomes contribute to carcinogenesis and disease progression in cancers of the skin, mouth, esophagus, lung, gastrointestinal, genital, blood, and lymph malignancy. We also insight into the molecular mechanisms of triggering, promoting, or inhibiting carcinogenesis and disease progress induced by microbiomes or/and their secretions of bioactive metabolites. And then, the strategies of application of microorganisms in cancer treatment were discussed in detail. However, the mechanisms by which human microbiomes function are still poorly understood. The bidirectional interactions between microbiotas and endocrine systems need to be clarified. Probiotics and prebiotics are believed to benefit human health via a variety of mechanisms, in particular, in tumor inhibition. It is largely unknown how microbial agents cause cancer or how cancer progresses. We expect this review may open new perspectives on possible therapeutic approaches of patients with cancer.

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Section: Human Carcinogenic or Cancer‐promoting Microbiomesmentioning

confidence: 99%

Section: 81mentioning

confidence: 99%

Human microbiomes in cancer development and therapy

Xia

Liu

et al. 2023

MedComm

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“…MHBSt 167 was one of the first reported mutations of S-truncated proteins, and MHBst 167 /HBx could induce nuclear factor-κB (NF-κB) activation via the PKC/ERK pathway in renal tubular cells [ 7 , 8 ]. The transcriptional activity of the c-Myc promoter could be upregulated by MHBst 167 , as well as transcription and translation of c‑Myc, which is a proto‑oncogene, in HepG2 cells [ 9 ]. The relationship between MHBSt 167 and HCC is unclear, and the mechanism remains to be determined.…”

Section: Introductionmentioning

confidence: 99%

MHBSt167 induced autophagy promote cell proliferation and EMT by activating the immune response in L02 cells

Cheng

Wang

Wei

et al. 2022

Virol J

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Background Hepatitis B virus can induce hepatocellular carcinoma (HCC) by inducing a host immune response against infected hepatocytes. C-terminally truncated middle surface protein (MHBSt) has been reported to contribute to HCC through transcriptional activation in epidemiology studies, while the underlying mechanism of MHBSt-induced HCC is unknown. Methods In this study, a premature stop at codon 167 in MHBS (MHBSt167) was investigated into eukaryotic expression plasmid pcDNA3.1(-). MHBSt167 expressed plasmid was transfected into the L02 cell line, cell proliferation was analyzed by CCK-8 and high-content screening assays, the cell cycle was analyzed by flow cytometry, and epithelial-to-mesenchymal transition and autophagy were analyzed by immunoblotting and immunofluorescence. NF-κB activation and the MHBSt167-induced immune response were analyzed by immunoblotting and immunofluorescence. IFN-α, IFN-β and IL-1α expression were analyzed by qPCR. Autophagy inhibitors were used to analyze the relationship between the immune response and autophagy. Results The results showed that MHBSt167 promoted L02 cell proliferation, accelerated cell cycle progression from the S to G2 phase and promoted epithelial-to-mesenchymal transition through ER-stress, leading to autophagy and NF-κB activation and increased immune-related factor expression. The MHBSt167-induced acceleration of cell proliferation and the cell cycle was abolished by autophagy or NF-κB inhibitors. Conclusion In summary, MHBSt167 could promote cell proliferation, accelerate cell cycle progression, induce EMT and activate autophagy through ER-stress to induce the host immune response, supporting a potential role of MHBSt167 in contributing to carcinogenesis.

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Transactivation of proto-oncogene c-Myc by hepatitis B virus transactivator MHBst167

Cited by 2 publications

References 16 publications

Human microbiomes in cancer development and therapy

Human microbiomes in cancer development and therapy

MHBSt167 induced autophagy promote cell proliferation and EMT by activating the immune response in L02 cells

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