Targeting PI3K/Akt signal transduction for cancer therapy

He, Yan; Sun, Miao; Zhang, Guo Geng; Yang, Jing; Chen, Kui Sheng; Xu, Wen; B, Li

doi:10.1038/s41392-021-00828-5

Cited by 401 publications

(279 citation statements)

References 271 publications

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“…The PI3K/AKT/mTOR signaling pathway is activated in many malignancies, including colorectal cancer, ovarian cancer, and breast cancer [ 8 ]. The PI3K/AKT signaling pathway could be activated by numerous stimuli, and the PI3K/AKT complex is the main cellular molecular pathway in autophagy [ 9 ].…”

Section: Introductionmentioning

confidence: 99%

BAP31 Promotes Proliferation, Invasion, and Metastasis of Liver Cancer Cells via Activating PI3K/AKT Pathway

Sun

Li²,

Wei³

et al. 2022

Journal of Healthcare Engineering

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Background. Many breakthroughs have been made in the clinical treatment of liver cancer, but there are still many liver cancer patients with limited treatment methods. Therefore, it is very important to find targets for early diagnosis and specific treatment of liver cancer. Methods. During the operation, 32 pairs of tumor tissues and corresponding normal liver tissues were acquired from patients. The mRNA expression was measured by qPCR. The protein expression was evaluated via Western blot. Flow cytometry assay was performed to measure the cells apoptosis. CCK-8 assay was performed to detect cell proliferation. Transwell chamber assay was applied to detect migration and invasion of SNU-449 cells. Results. BAP31 was upregulated in liver cancer tissues and cells. Knockdown of BAP31 repressed cell proliferation and enhanced cell apoptosis of liver cancer. Knockdown of BAP31 apparently upregulated apoptosis-related proteins (Bax and Caspase-3), while it downregulated antiapoptotic proteins (Bcl-2). Knockdown of BAP31 repressed migration and invasion of SNU-449 cells. In contrast with the control and si-NC group, protein expression of MMP-2 and MMP-9 was obviously lower after si-BAP31 transfection of cells. Knockdown of BAP31 repressed PI3K/AKT signaling pathways in liver cancer cells. Conclusion. Knockdown of BAP31 repressed cell proliferation, migration, and invasion in liver cancer by suppressing PI3K/AKT/mTOR signaling pathways.

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Section: Introductionmentioning

confidence: 99%

BAP31 Promotes Proliferation, Invasion, and Metastasis of Liver Cancer Cells via Activating PI3K/AKT Pathway

Sun

Li²,

Wei³

et al. 2022

Journal of Healthcare Engineering

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“…PI3K/AKT signaling axis is integral to tumor progression owing to its ability to enhance mobility and reduce intercellular adhesion ( 25 ). The EMT process and associated loss of epithelial cell phenotypes can be regulated in response to particular extracellular signaling molecules, with cell surface receptors and transcription factors ultimately transducing these signals to alter cellular characteristics ( 26 , 27 ). The PI3K/AKT/GSK3β/Snail signaling has previously been shown to be critical to tumor metastasis via the modulation of EMT induction in multiple cancers ( 28 – 30 ).…”

Section: Discusionmentioning

confidence: 99%

Extracellular Matrix Protein 1 Regulates Colorectal Cancer Cell Proliferative, Migratory, Invasive and Epithelial-Mesenchymal Transition Activities Through the PI3K/AKT/GSK3β/Snail Signaling Axis

et al. 2022

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In prior reports, extracellular matrix protein 1 (ECM1) upregulation has been reported in colorectal cancer (CRC) patient tumor tissues, and has been suggested to be related to the metastatic progression of CRC, although the underlying mechanisms have yet to be clarified. In this study, we found that ECM1 was overexpressed in both CRC tissues and cell lines. Upregulation of ECM1 was correlated with tumor size, lymph node status and TNM stage in CRC patients. Knocking down ECM1 suppressed CRC cell growth, migration and invasion, in addition to reducing the expression of Vimentin and increasing E-cadherin expression. The overexpression of ECM1, in contrast, yielded the opposite phenotypic outcomes while also promoting the expression of p-AKT, p-GSK3β, and Snail, which were downregulated when ECM1 was knocked down. Treatment with LY294002 and 740 Y-P reversed the impact upregulation and downregulation of ECM1 on CRC cell metastasis and associated EMT induction. In vivo analyses confirmed that ECM1 overexpression was able to enhance EMT induction and CRC tumor progression. In conclusion, ECM1 influences CRC development and progression in an oncogenic manner, and regulates CRC metastasis and EMT processes via the PI3K/AKT/GSK3β/Snail signaling axis.

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“…Our results demonstrated that the n-10 fatty acid family is able to influence the EGFR/AKT/mTOR cascade, which is a fundamental pathway ubiquitously present in tumors to maintain growth, survival, and metastasis [ 34 , 35 ]. EGFR is overexpressed in more than 20% of metastatic breast cancer cases and approximately half of TNBC cases [ 36 ].…”

Section: Discussionmentioning

confidence: 99%

Sapienic Acid Metabolism Influences Membrane Plasticity and Protein Signaling in Breast Cancer Cell Lines

Kucuksayan

Sansone

Chatgilialoglu

et al. 2022

Cells

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The importance of sapienic acid (6c-16:1), a monounsaturated fatty acid of the n-10 family formed from palmitic acid by delta-6 desaturase, and of its metabolism to 8c-18:1 and sebaleic acid (5c,8c-18:2) has been recently assessed in cancer. Data are lacking on the association between signaling cascades and exposure to sapienic acid comparing cell lines of the same cancer type. We used 50 μM sapienic acid supplementation, a non-toxic concentration, to cultivate MCF-7 and 2 triple-negative breast cancer cells (TNBC), MDA-MB-231 and BT-20. We followed up for three hours regarding membrane fatty acid remodeling by fatty acid-based membrane lipidome analysis and expression/phosphorylation of EGFR (epithelial growth factor receptor), mTOR (mammalian target of rapamycin) and AKT (protein kinase B) by Western blotting as an oncogenic signaling cascade. Results evidenced consistent differences among the three cell lines in the metabolism of n-10 fatty acids and signaling. Here, a new scenario is proposed for the role of sapienic acid: one based on changes in membrane composition and properties, and the other based on changes in expression/activation of growth factors and signaling cascades. This knowledge can indicate additional players and synergies in breast cancer cell metabolism, inspiring translational applications of tailored membrane lipid strategies to assist pharmacological interventions.

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Targeting PI3K/Akt signal transduction for cancer therapy

Cited by 401 publications

References 271 publications

BAP31 Promotes Proliferation, Invasion, and Metastasis of Liver Cancer Cells via Activating PI3K/AKT Pathway

BAP31 Promotes Proliferation, Invasion, and Metastasis of Liver Cancer Cells via Activating PI3K/AKT Pathway

Extracellular Matrix Protein 1 Regulates Colorectal Cancer Cell Proliferative, Migratory, Invasive and Epithelial-Mesenchymal Transition Activities Through the PI3K/AKT/GSK3β/Snail Signaling Axis

Sapienic Acid Metabolism Influences Membrane Plasticity and Protein Signaling in Breast Cancer Cell Lines

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