Research Progress on the Effects of PI3K/Akt Pathway on Immune Escape

Tianran Wang

doi:10.54097/qmdmmy81

Authors

Tianran Wang

DOI:

https://doi.org/10.54097/qmdmmy81

Keywords:

PI3K/Akt Pathway; Immune Escape; Cell Apoptosis; T Cell Activation; Cancer Treatment.

Abstract

The PI3K/Akt pathway can promote immune escape in tumors, making cancer cells more difficult for the immune system to attack. It is usually possible to regulate the number and function of immune cells by inhibiting apoptosis and T cell activation, and generate immune escape mutations to make cancer cells more resistant to immune monitoring. In-depth understanding of the role of PI3K/Akt pathway in immune escape will help to reveal the mechanism of tumor development, improve the effectiveness of cancer treatment. development, improve the effectiveness of cancer treatment, and restore the immune system's monitoring and attack on cancer cells by inhibiting the activity of PI3K/Akt. In this review, we review the research progress on the effects of G protein-coupled receptor-activated PI3K/Akt pathway on immune escape. This review aims to summarize domestic and international studies that reveal how the PI3K/Akt pathway plays a key role in immune escape, and through in-depth understanding of the role of the PI3K/Akt pathway in immune escape. This review aims to summarize domestic and international studies that reveal how the PI3K/Akt pathway plays a key role in immune escape, and through in-depth understanding of the molecular mechanism, new therapeutic targets can be identified. Scientists from abroad have explored various cancer forms, such as lung, ovarian, and endometrial cancers, etc., so as to provide targeted treatment strategies and increase the applicability of immunotherapy for different cancers; By studying the role of PI3K/Akt pathway, we can explore the potential application of PI3K/Akt pathway for different cancers. By studying the role of PI3K/Akt pathway, we can explore the potential application of existing drugs or new drugs in immunotherapy, so as to improve the diversity of treatment. techniques are combined with clinical data to discover associations between the PI3K/Akt pathway and treatment response in patients to support personalized medicine. Current studies have found that the PI3K/Akt pathway is a key mechanism for immune monitoring of tumor cell escape, and in-depth study of its role is expected to improve the quality of treatment. Current studies have found that the PI3K/Akt pathway is a key mechanism for immune monitoring of tumor cell escape, and in-depth study of its role is expected to improve current immunotherapy strategies and improve patient survival. In the future, whether there are new therapeutic opportunities for PI3K/Akt pathway in immune escape studies, so as to help optimize cancer treatment strategies, improve the efficacy of immunotherapy in future, whether there are new therapeutic opportunities for PI3K/Akt pathway in immune escape studies, so as to help optimize cancer treatment strategies, improve the efficacy of immunotherapy, and improve patient treatment outcomes.

Downloads

Download data is not yet available.

References

[1] Liu H. et al. Necroptosis-related prognostic model for pancreatic carcinoma reveals its invasion and metastasis potential through hybrid EMT and immune escape[J]. Biomedicines, 2023, 11(6): 1738.

[2] Sharma V. et al. Recent nanotechnological interventions targeting PI3K/Akt/mTOR pathway: A focus on breast cancer[J]. Seminars in Cancer Biology, 2019, 59133-146.

[3] Chai C. et al. BCR-ABL1-driven exosome-miR130b-3p-mediated gap-junction Cx43 MSC intercellular communications imply therapies of leukemic subclonal evolution [J]. Theranostics, 2023, 13(12): 3943.

[4] Shen H. et al. Overcoming MTDH and MTDH-SND1 complex: driver and potential therapeutic target of cancer[J]. Cancer Insight, 2023, 3(1): 55-82.

[5] Huang Xulan et al. Progress in the relationship between PI3K/Akt signaling pathway and tumor cell apoptosis[J]. Cancer, 2008,27(03):331-336.

[6] Zhang Y C. et al. What role does PDL1 play in EMT changes in tumors and fibrosis? [J]. Frontiers in Immunology, 2023, 14: 1226038.

[7] Guo C. et al. FGF19/FGFR4 signaling contributes to hepatocellular carcinoma survival and immune escape by regulating IGF2BP1-mediated expression of PD-L1[J]. Biomedicine & Pharmacotherapy, 2024, 170: 115955.

[8] Altomare DA. et al. AKT and mTOR phosphorylation is frequently detected in ovarian cancer and can be targeted to disrupt ovarian tumor cell growth[J]. Oncogene, 2004,23:5853-5857.

[9] Abu-Eid, R. et al. Selective Inhibition of Regulatory T Cells by Targeting the PI3K/Akt Pathway[J]. Cancer Immunol Research, 2014,2(11):1080-1089.

[10] Rui Z. et al. PD-1/PD-L1 blockade rescue exhausted CD8+ T cells in gastrointestinal stromal tumours via the PI3K/ Akt/ m TOR signalling pathway[J]. Cell proliferation, 2019, 52 (3): e 12571.

[11] Hussain S. et al. Regulation of cancer progression by CK2: an emerging therapeutic target[J]. Medical Oncology, 2024, 41(5): 94.

[12] Marijt, K. A. et al. Metabolic stress in cancer cells induces immune escape through a PI3K-dependent blockade of IFNγ receptor signaling[J]. Journal for ImmunoTherapy of Cancer, 2019,7(1):1-12.

[13] Kim, E.H., Suresh, M. Role of PI3K/Akt signaling in memory CD8 T cell differentiation[J]. Frontiers in Immunology, 2013, 420.

[14] Noh, K.H. et al. Activation of Akt as a Mechanism for Tumor Immune Evasion[J]. Molecular Therapy, 2009,17(3):439-447.

[15] Ding J. et al. DNA polymerase ζ suppresses the radiosensitivity of glioma cells by regulating the PI3K/AKT/mTOR pathway[J]. Autoimmunity, 2023, 56(1): 2234101.

[16] Stephan Sauer. et al. T cell receptor signaling controls Foxp3 expression via PI3K, Akt, and mTOR[J]. PNAS, 2008,105 (22): 7797-7802.

[17] Herrero-Sánchez C M. et al. Targeting of PI3K/AKT/mTOR pathway to inhibit T cell activation and prevent graft-versus-host disease development[J]. Journal of Hematology Oncology, 2016,9(1):1-14.

[18] Wan, J. et al. Low dose photodynamic-therapy induce immune escape of tumor cells in a HIF-1α dependent manner through PI3K/Akt pathway[J].International Immunopharmacology, 2015, 28 (1):44-51.

[19] David A. Fruman. et al. Fine tuning the immune response with PI3K [J]. Immunological reviews, 2009,228(1):253-72.

[20] Li Yunyun et al. Progress in the study of PI3K/AKT and JAK/STAT signaling pathways and IDO-mediated immune escape mechanism in endometrial cancer[J]. Oncology, 2013, 33 (07):658-662.

[21] Dai, Y.L. et al. Vemurafenib inhibits immune escape biomarker BCL2A1 by targeting PI3K/AKT signaling pathway to suppress breast cancer[J]. Frontiers in Oncology, 2022, 1290 6197-906197.

[22] Zhenghang W. et al. Mutations of PI3K-AKT-mTOR pathway as predictors for immune cell infiltration and immunotherapy efficacy in dMMR/MSI-H gastric adenocarcinoma[J]. BMC Medicine, 2022,20(1):133-133.

[23] Wu Xiao. Helicobacter pylori-induced IL-8 promotes immune escape from gastric cancer by up-regulating PD-L1 expression through PI3K/AKT signaling pathway[D]. Anhui Medical University, 2021.

[24] Chen Yani. INPP4B inhibits glioma proliferation and immune escape through inhibiting PI3K/AKT signaling pathway[D]. Hubei Medical College, 2023.

[25] CHEN Z. et al. Progress on the pathological roles of immune checkpoint CD276 protein in tumorigenesis and development [J]. Basic & Clinical Medicine, 2023,43(7): 1143.

[26] HAHNE, J.C. et al. Immune escape of AKT overexpressing ovarian cancer cells[J]. International Journal of Oncology, 2013,42(5):1630-1635.