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      • Record: found
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      STEAP4 inhibits cisplatin-induced chemotherapy resistance through suppressing PI3K/AKT in hepatocellular carcinoma

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          Abstract

          Chemotherapy resistance is the leading cause for hepatocellular carcinoma (HCC)-induced death. Exploring resistance generation mechanism is an urgent need for HCC therapy. Here, we found STEAP4 was significantly downregulated in HCC patients with recurrence. Patients with low STEAP4 had poor outcome, suggesting STEAP4 might inhibit chemotherapy resistance. Cell viability assay, colony formation assay, apoptosis assay, soft agar growth assay, and tumor animal model showed STEAP4 inhibited cisplatin resistance. Mechanism analysis showed STEAP4 inhibited PI3K/AKT pathway through directly interacting with AKT. Double knockdown of STEP4 and AKT significantly inhibited cisplatin resistance. We also found STEAP4 expression was negatively correlated with PI3K/AKT pathway activity in clinic specimens. In summary, our findings suggested STEAP4 inhibited cisplatin resistance through suppressing PI3K/AKT pathway activity, providing a target for HCC therapy.

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          Regorafenib for patients with hepatocellular carcinoma who progressed on sorafenib treatment (RESORCE): a randomised, double-blind, placebo-controlled, phase 3 trial.

          Jordi Bruix, Shukui Qin, Philippe Merle … (2017)
          There are no systemic treatments for patients with hepatocellular carcinoma (HCC) whose disease progresses during sorafenib treatment. We aimed to assess the efficacy and safety of regorafenib in patients with HCC who have progressed during sorafenib treatment.
          Article 0 comments Cited 971 times – based on 0 reviews     Review now
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            AKT/PKB Signaling: Navigating the Network

            Brendan D Manning, Alex Toker (2017)
            The Ser/Thr kinase AKT, also known as protein kinase B (PKB), was discovered 25 years ago and has been the focus of tens of thousands of studies in diverse fields of biology and medicine. There have been many advances in our knowledge of the upstream regulatory inputs into AKT, key multifunctional downstream signaling nodes (GSK3, FoxO, mTORC1), which greatly expand the functional repertoire of Akt, and the complex circuitry of this dynamically branching and looping signaling network that is ubiquitous to nearly every cell in our body. Mouse and human genetic studies have also revealed physiological roles for the AKT network in nearly every organ system. Our comprehension of AKT regulation and functions is particularly important given the consequences of AKT dysfunction in diverse pathological settings, including developmental and overgrowth syndromes, cancer, cardiovascular disease, insulin resistance and type-2 diabetes, inflammatory and autoimmune disorders, and neurological disorders. There has also been much progress in developing AKT-selective small molecule inhibitors. Improved understanding of the molecular wiring of the AKT signaling network continues to make an impact that cuts across most disciplines of the biomedical sciences.
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              New knowledge of the mechanisms of sorafenib resistance in liver cancer

              Yan-jing Zhu, Bo Zheng, Hong-yang Wang … (2017)
              Sorafenib is an oral multikinase inhibitor that suppresses tumor cell proliferation and angiogenesis and promotes tumor cell apoptosis. It was approved by the FDA for the treatment of advanced renal cell carcinoma in 2006, and as a unique target drug for advanced hepatocellular carcinoma (HCC) in 2007. Sorafenib can significantly extend the median survival time of patients but only by 3–5 months. Moreover, it is associated with serious adverse side effects, and drug resistance often develops. Therefore, it is of great importance to explore the mechanisms underlying sorafenib resistance and to develop individualized therapeutic strategies for coping with these problems. Recent studies have revealed that in addition to the primary resistance, several mechanisms are underlying the acquired resistance to sorafenib, such as crosstalk involving PI3K/Akt and JAK-STAT pathways, the activation of hypoxia-inducible pathways, and epithelial-mesenchymal transition. Here, we briefly describe the function of sorafenib, its clinical application, and the molecular mechanisms for drug resistance, especially for HCC patients.
              Article 0 comments Cited 209 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Jianting Long: longjt2@mail.sysu.edu.cn
                Xuewei Yang: yangxw0908@163.com
                Heping Li: liheping@mail.sysu.edu.cn
                Journal
                Journal ID (nlm-ta): Cancer Metab
                Journal ID (iso-abbrev): Cancer Metab
                Title: Cancer & Metabolism
                Publisher: BioMed Central (London )
                ISSN (Electronic): 2049-3002
                Publication date (Electronic): 18 December 2023
                Publication date PMC-release: 18 December 2023
                Publication date Collection: 2023
                Volume: 11
                Electronic Location Identifier: 26
                Affiliations
                [1 ]Department of Hepatobiliary Surgery, the First Affiliated Hospital of Gannan Medical University, ( https://ror.org/040gnq226) Ganzhou, 341000 People’s Republic of China
                [2 ]Ganzhou Key Laboratory of Hepatocellular Carcinoma, the First Affiliated Hospital of Gannan Medical University, ( https://ror.org/040gnq226) Ganzhou, 341000 People’s Republic of China
                [3 ]Department of Hepatobiliary Surgery, The First Affiliated Hospital of Sun Yat-sen University, ( https://ror.org/037p24858) Guangzhou, 510080 People’s Republic of China
                [4 ]Department of Medical Oncology, The First Affiliated Hospital of Sun Yat-sen University, ( https://ror.org/037p24858) Guangzhou, 510080 People’s Republic of China
                [5 ]Department of Clinical Research Center, the First Affiliated Hospital of Gannan Medical University, ( https://ror.org/040gnq226) Ganzhou, 341000 People’s Republic of China
                [6 ]Department of Hepatobiliary Surgery, the Second Affiliated Hospital of Guangzhou Medical University, ( https://ror.org/00a98yf63) Guangzhou, 510000 People’s Republic of China
                Article
                Publisher ID: 323
                DOI: 10.1186/s40170-023-00323-1
                PMC ID: 10726618
                PubMed ID: 38111065
                SO-VID: 3780b884-0ca8-4a9a-a62e-ebdf025ccf12
                Copyright © © The Author(s) 2023
                License:

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

                History
                Date received : 16 June 2023
                Date accepted : 4 November 2023
                Categories
                Subject: Research
                Custom metadata
                issue-copyright-statement © BioMed Central Ltd., part of Springer Nature 2023

                Keywords: stepa4,chemotherapy resistance,akt,hepatocellular carcinoma
                Data availability:
                Keywords: stepa4, chemotherapy resistance, akt, hepatocellular carcinoma

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