FOXS1 promotes prostate cancer progression through the Hedgehog/Gli1 pathway

Wang, Minyu; Huang, Wanying

doi:10.1016/j.bcp.2023.115893

Cited by 4 publications

(2 citation statements)

References 33 publications

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“…119 , 120 Forkhead box S1 (FOXS1) is a member of FOX TFs that can modulate EMT and is correlated with poor prognosis of tumor. 121 , 122 FOXS1 can inhibit the ubiquitination of GLI1 to upregulate Hedgehog/GLI1 signaling, which leads to tumor metastasis via inducing EMT. 122 Besides, Hedgehog/GLI is reported to act with Notch signaling in colorectal cancer cells to drive EMT to promote tumor invasiveness.…”

Section: Signaling Pathways Regulating Empmentioning

confidence: 99%

“… 121 , 122 FOXS1 can inhibit the ubiquitination of GLI1 to upregulate Hedgehog/GLI1 signaling, which leads to tumor metastasis via inducing EMT. 122 Besides, Hedgehog/GLI is reported to act with Notch signaling in colorectal cancer cells to drive EMT to promote tumor invasiveness. 123 Moreover, Hippo signaling pathway also participates in the modulation of EMT, the main effector downstream of which is the YAP.…”

Section: Signaling Pathways Regulating Empmentioning

confidence: 99%

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Epithelial–mesenchymal plasticity in cancer: signaling pathways and therapeutic targets

Wang,

Xue,

Pang

et al. 2024

MedComm

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Currently, cancer is still a leading cause of human death globally. Tumor deterioration comprises multiple events including metastasis, therapeutic resistance and immune evasion, all of which are tightly related to the phenotypic plasticity especially epithelial–mesenchymal plasticity (EMP). Tumor cells with EMP are manifest in three states as epithelial–mesenchymal transition (EMT), partial EMT, and mesenchymal–epithelial transition, which orchestrate the phenotypic switch and heterogeneity of tumor cells via transcriptional regulation and a series of signaling pathways, including transforming growth factor‐β, Wnt/β‐catenin, and Notch. However, due to the complicated nature of EMP, the diverse process of EMP is still not fully understood. In this review, we systematically conclude the biological background, regulating mechanisms of EMP as well as the role of EMP in therapy response. We also summarize a range of small molecule inhibitors, immune‐related therapeutic approaches, and combination therapies that have been developed to target EMP for the outstanding role of EMP‐driven tumor deterioration. Additionally, we explore the potential technique for EMP‐based tumor mechanistic investigation and therapeutic research, which may burst vigorous prospects. Overall, we elucidate the multifaceted aspects of EMP in tumor progression and suggest a promising direction of cancer treatment based on targeting EMP.

show abstract

Section: Signaling Pathways Regulating Empmentioning

confidence: 99%

Section: Signaling Pathways Regulating Empmentioning

confidence: 99%

Epithelial–mesenchymal plasticity in cancer: signaling pathways and therapeutic targets

Wang,

Xue,

Pang

et al. 2024

MedComm

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Combined targeting of Hedgehog/GLI1 and Wnt/β‐catenin pathways in mantle cell lymphoma

Han,

Li,

Liu

et al. 2024

Hematological Oncology

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Mantle cell lymphoma (MCL) is a rare and aggressive form of non‐Hodgkin lymphoma. Challenges in its treatment include relapse, drug resistance, and a short survival period. The Hedgehog/GLI1 (Hh/GLI1) and Wnt/β‐catenin pathways are crucial in cancer cell proliferation, survival, and drug resistance, making them significant targets for anticancer research. This study aimed to assess the effectiveness of combining inhibitors for both pathways against MCL and investigate the underlying molecular mechanisms. The co‐expression of key proteins from the Hh/GLI1 and Wnt/β‐catenin pathways was observed in MCL. Targeting the Hh/GLI1 pathway with the GLI1 inhibitor GANT61 and the Wnt/β‐catenin pathway with the CBP/β‐catenin transcription inhibitor ICG‐001, dual‐target therapy was demonstrated to synergistically suppressed the activity of MCL cells. This approach promoted MCL cell apoptosis, induced G0/G1 phase blockade, decreased the percentage of S‐phase cells, and enhanced the sensitivity of MCL cells to the drugs adriamycin and ibrutinib. Both GANT61 and ICG‐001 downregulated GLI1 and β‐catenin while upregulating GSK‐3β expression. The interaction between Hh/GLI1 and Wnt/β‐catenin pathways was mediated by GANT61‐dependent Hh/GLI1 inhibition. Moreover, GLI1 knockdown combined with ICG‐001 synergistically induced apoptosis and increased drug sensitivity of MCL cells to doxorubicin and ibrutinib. GANT61 attenuated the overexpression of β‐catenin and decreased the inhibition of GSK‐3β in MCL cells. Overall, the combined targeting of both the Hh/GLI1 and Wnt/β‐catenin pathways was more effective in suppressing proliferation, inducing G0/G1 cycle retardation, promoting apoptosis, and increasing drug sensitivity of MCL cells than mono treatments. These findings emphasize the potential of combinatorial therapy for treating MCL patients.

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Targeting GLI1 and BAX by nanonoscapine could impede prostate adenocarcinoma progression

Nazari,

Heidarian,

Masoudnia

et al. 2024

Sci Rep

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FOXS1 promotes prostate cancer progression through the Hedgehog/Gli1 pathway

Cited by 4 publications

References 33 publications

Epithelial–mesenchymal plasticity in cancer: signaling pathways and therapeutic targets

Epithelial–mesenchymal plasticity in cancer: signaling pathways and therapeutic targets

Combined targeting of Hedgehog/GLI1 and Wnt/β‐catenin pathways in mantle cell lymphoma

Targeting GLI1 and BAX by nanonoscapine could impede prostate adenocarcinoma progression

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