Overview of hepatocellular carcinoma: from molecular aspects to future therapeutic options

Panneerselvam, Sugan; Wilson, Cornelia; Kumar, Prem; Abirami, Dinu; Pamarthi, Jayakrishna; Reddy, Mettu Srinivas; Varghese, Joy

doi:10.1080/19336918.2023.2258539

Cited by 7 publications

(3 citation statements)

References 162 publications

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“…Depletion of p53-a tumor suppressor protein-favors the regression of the differentiation of mature hepatocytes into progenitor cells. The alteration in the formation of HCC, followed by a genetic mutation in the Wnt and Notch signaling pathways, acts mainly in the development of embryonic cells, coordinating cell differentiation, cell proliferation, and apoptosis [221].…”

Section: Mafld and The Development Of Hepatocellular Carcinomamentioning

confidence: 99%

Underlying Mechanisms behind the Brain–Gut–Liver Axis and Metabolic-Associated Fatty Liver Disease (MAFLD): An Update

De Cól,

de Lima,

Pompeu

et al. 2024

IJMS

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Metabolic-associated fatty liver disease (MAFLD) includes several metabolic dysfunctions caused by dysregulation in the brain–gut–liver axis and, consequently, increases cardiovascular risks and fatty liver dysfunction. In MAFLD, type 2 diabetes mellitus, obesity, and metabolic syndrome are frequently present; these conditions are related to liver lipogenesis and systemic inflammation. This study aimed to review the connection between the brain–gut–liver axis and MAFLD. The inflammatory process, cellular alterations in hepatocytes and stellate cells, hypercaloric diet, and sedentarism aggravate the prognosis of patients with MAFLD. Thus, to understand the modulation of the physiopathology of MAFLD, it is necessary to include the organokines involved in this process (adipokines, myokines, osteokines, and hepatokines) and their clinical relevance to project future perspectives of this condition and bring to light new possibilities in therapeutic approaches. Adipokines are responsible for the activation of distinct cellular signaling in different tissues, such as insulin and pro-inflammatory cytokines, which is important for balancing substances to avoid MAFLD and its progression. Myokines improve the quantity and quality of adipose tissues, contributing to avoiding the development of MAFLD. Finally, hepatokines are decisive in improving or not improving the progression of this disease through the regulation of pro-inflammatory and anti-inflammatory organokines.

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Section: Mafld and The Development Of Hepatocellular Carcinomamentioning

confidence: 99%

Underlying Mechanisms behind the Brain–Gut–Liver Axis and Metabolic-Associated Fatty Liver Disease (MAFLD): An Update

De Cól,

de Lima,

Pompeu

et al. 2024

IJMS

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“…Gut microbiota dysbiosis, together with altered metabolite profiles and compromised gut barrier integrity, profoundly disrupts immune homeostasis in the liver and consequently fosters carcinogenesis. Clinical studies have revealed augmented numbers of regulatory T cells and diminished numbers of CD3+ and CD8+ T cells in the peripheral blood and tumor specimens of patients with HCC-findings correlated with poorer prognosis [117][118][119] . Modulation of the gut microbiota has potential to reinvigorate anti-tumor responses.…”

Section: Gut Microbiota Dysbiosis and Hccmentioning

confidence: 99%

Bile acids, gut microbiota, and therapeutic insights in hepatocellular carcinoma

Song,

Lau,

Zhang

et al. 2023

Cancer Biol Med

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Hepatocellular carcinoma (HCC) is a prevalent and aggressive liver malignancy. The interplay between bile acids (BAs) and the gut microbiota has emerged as a critical factor in HCC development and progression. Under normal conditions, BA metabolism is tightly regulated through a bidirectional interplay between gut microorganisms and BAs. The gut microbiota plays a critical role in BA metabolism, and BAs are endogenous signaling molecules that help maintain liver and intestinal homeostasis. Of note, dysbiotic changes in the gut microbiota during pathogenesis and cancer development can disrupt BA homeostasis, thereby leading to liver inflammation and fibrosis, and ultimately contributing to HCC development. Therefore, understanding the intricate interplay between BAs and the gut microbiota is crucial for elucidating the mechanisms underlying hepatocarcinogenesis. In this review, we comprehensively explore the roles and functions of BA metabolism, with a focus on the interactions between BAs and gut microorganisms in HCC. Additionally, therapeutic strategies targeting BA metabolism and the gut microbiota are discussed, including the use of BA agonists/antagonists, probiotic/prebiotic and dietary interventions, fecal microbiota transplantation, and engineered bacteria. In summary, understanding the complex BA-microbiota crosstalk can provide valuable insights into HCC development and facilitate the development of innovative therapeutic approaches for liver malignancy.

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“…HBV is the main etiological factor associated with HCC in India. But right now, India lacks access to thorough HCC data [3].…”

Section: Introductionmentioning

confidence: 99%

Molecular Interaction Study between Gentamicin and the Cancer Protein Target (TP53) using in silico Tools

Priyadharshini M.,

Leelavathi,

Tanzeem Azeeza S.

2024

UPJOZ

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The most prevalent mutation in hepatocellular carcinoma (HCC), TP53 mutations impacts the course and prognosis of HCC. 3D in silico drug docking techniques were employed to make the possible mutant target tumor protein 53 (TP53) interact with benzene acetic acid (Gentamicin) and non-steroidal anti-inflammatory drugs (NSAIDs). To carry out drug docking techniques, the translated amino acid sequence and three-dimensional chemical compound were obtained from the NCBI database. The use of sophisticated 3D molecular visualization tools was employed in post-docking experiments. The docking study results unequivocally show that gentamicin directly suppresses amino acid mutational sites. TP53 and Gentamicin's electrostatic force is depicted in a three-dimensional manner using notions from molecular dynamics techniques. In the end, it was determined that gentamicin, an Antibiotic medication, helps treat liver cancer. Most chemotherapy medications cause pain. Therefore, Gentamicin shall be used to lessen discomfort while minimizing the symptoms of cancer.

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Overview of hepatocellular carcinoma: from molecular aspects to future therapeutic options

Cited by 7 publications

References 162 publications

Underlying Mechanisms behind the Brain–Gut–Liver Axis and Metabolic-Associated Fatty Liver Disease (MAFLD): An Update

Underlying Mechanisms behind the Brain–Gut–Liver Axis and Metabolic-Associated Fatty Liver Disease (MAFLD): An Update

Bile acids, gut microbiota, and therapeutic insights in hepatocellular carcinoma

Molecular Interaction Study between Gentamicin and the Cancer Protein Target (TP53) using in silico Tools

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