Wnt signaling pathway in cancer immunotherapy

Zhou, Yang; Jiang, Xu; Luo, Haichang; Meng, Xiangjing; Chen, Ming; Zhu, Di

doi:10.1016/j.canlet.2021.10.034

Cited by 111 publications

(57 citation statements)

References 140 publications

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“…T regulatory cells (Tregs) in colon cancer patients can become pro-inflammatory and tumor-promoting [ 62 ]. RORγt is a marker transcription factor of T helper 17 (T(H)17) cells.…”

Section: Wnt Pathway-related Biochemical Processmentioning

confidence: 99%

Wnt signaling in colorectal cancer: pathogenic role and therapeutic target

et al. 2022

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Background The Wnt signaling pathway is a complex network of protein interactions that functions most commonly in embryonic development and cancer, but is also involved in normal physiological processes in adults. The canonical Wnt signaling pathway regulates cell pluripotency and determines the differentiation fate of cells during development. The canonical Wnt signaling pathway (also known as the Wnt/β-catenin signaling pathway) is a recognized driver of colon cancer and one of the most representative signaling pathways. As a functional effector molecule of Wnt signaling, the modification and degradation of β-catenin are key events in the Wnt signaling pathway and the development and progression of colon cancer. Therefore, the Wnt signaling pathway plays an important role in the pathogenesis of diseases, especially the pathogenesis of colorectal cancer (CRC). Objective Inhibit the Wnt signaling pathway to explore the therapeutic targets of colorectal cancer. Methods Based on studying the Wnt pathway, master the biochemical processes related to the Wnt pathway, and analyze the relevant targets when drugs or inhibitors act on the Wnt pathway, to clarify the medication ideas of drugs or inhibitors for the treatment of diseases, especially colorectal cancer. Results Wnt signaling pathways include: Wnt/β-catenin or canonical Wnt signaling pathway, planar cell polarity (Wnt-PCP) pathway and Wnt-Ca2+ signaling pathway. The Wnt signaling pathway is closely related to cancer cell proliferation, stemness, apoptosis, autophagy, metabolism, inflammation and immunization, microenvironment, resistance, ion channel, heterogeneity, EMT/migration/invasion/metastasis. Drugs/phytochemicals and molecular preparations for the Wnt pathway of CRC treatment have now been developed. Wnt inhibitors are also commonly used clinically for the treatment of CRC. Conclusion The development of drugs/phytochemicals and molecular inhibitors targeting the Wnt pathway can effectively treat colorectal cancer clinically.

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“…T regulatory cells (Tregs) in colon cancer patients can become pro-inflammatory and tumor-promoting [ 62 ]. RORγt is a marker transcription factor of T helper 17 (T(H)17) cells.…”

Section: Wnt Pathway-related Biochemical Processmentioning

confidence: 99%

Wnt signaling in colorectal cancer: pathogenic role and therapeutic target

et al. 2022

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“…The appearance of CTNNB1 S45F mutation in ctDNA is remarkable since aberrant WNT signaling is associated with impaired anticancer immunity and considered a key contributor to tumor progression and resistance to checkpoint inhibitors. [10][11][12] Indeed, tumor cell-intrinsic WNT/β-catenin signaling has been shown to prevent antitumor immunity in melanoma 13 and in hepatocarcinoma. 14,15 Furthermore, Luke et al 16 profiled the correlation of WNT/β-catenin signaling and the T-cell-inflamed tumor microenvironment across The Cancer Genome Atlas and showed a pan-cancer association of this signaling pathway with immune exclusion.…”

Section: Discussionmentioning

confidence: 99%

Acquired Resistance Mechanisms to PD-L1 Blockade in a Patient With Microsatellite Instability-High Extrahepatic Cholangiocarcinoma

Niger

Nichetti

Dell'Angelo

et al. 2022

JCO Precision Oncology

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“…Conversely, the overexpression of SEMA6A activated the Wnt/β-catenin pathway, which could be reversed by pharmacological β-catenin inhibition. Also, βcatenin is a multifunctional protein encoded by the CTNNB1 gene that mediates signal transduction and exerts a core role in promoting tumor proliferation and metastasis in various malignancies 31 . Although SEMA6A knockdown inhibited the activity of the Wnt/β-catenin pathway, the mRNA level of β-catenin was not affected.…”

Section: Discussionmentioning

confidence: 99%

VHL-HIF-2α axis-induced SEMA6A upregulation stabilized β-catenin to drive clear cell renal cell carcinoma progression

Ji¹,

Xu²,

Xie³

et al. 2022

Preprint

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SEMA6A is a multifunctional transmembrane semaphorin protein that participates in various cellular processes, including axon guidance, cell migration, and cancer progression. However, the role of SEMA6A in clear cell renal cell carcinoma (ccRCC) is unclear. Based on high-throughput sequencing data, here we report that SEMA6A is a novel target gene of the VHL-HIF-2α axis and overexpressed in ccRCC. Chromatin immunoprecipitation and reporter assays revealed that HIF-2α directly activated SEMA6A transcription in hypoxic ccRCC cells. Wnt/β-catenin pathway activation is correlated with the expression of SEMA6A in ccRCC; the latter physically interacted with SEC62 and promoted ccRCC progression through SEC62-dependent β-catenin stabilization and activation. Depletion of SEMA6A impaired HIF-2α-induced Wnt/β-catenin pathway activation and led to defective ccRCC cell proliferation both in vitro and in vivo. SEMA6A overexpression promoted the malignant phenotypes of ccRCC, which was reversed by SEC62 depletion. Collectively, this study revealed a potential role for VHL-HIF-2α-SEMA6A-SEC62 axis in the activation of Wnt/β-catenin pathway. Thus, SEMA6A may act as a potential therapeutic target, especially in VHL-deficient ccRCC.

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Wnt signaling pathway in cancer immunotherapy

Cited by 111 publications

References 140 publications

Wnt signaling in colorectal cancer: pathogenic role and therapeutic target

Wnt signaling in colorectal cancer: pathogenic role and therapeutic target

Acquired Resistance Mechanisms to PD-L1 Blockade in a Patient With Microsatellite Instability-High Extrahepatic Cholangiocarcinoma

VHL-HIF-2α axis-induced SEMA6A upregulation stabilized β-catenin to drive clear cell renal cell carcinoma progression

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