Overexpressed FAM111B degrades GSDMA to promote esophageal cancer tumorigenesis and cisplatin resistance

Wang, Haiqin; Wang, Haohui; Chen, Jiajing; Liu, Pian; Xiao, Xiaoxiong

doi:10.1007/s13402-023-00871-0

Cited by 5 publications

(2 citation statements)

References 38 publications

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“…Additionally, our protein transcriptomics investigation revealed that the FAM111B-MYC axis may facilitate oncogenic proliferation by modulating genetic information processing. Notably, FAM111B has been implicated in DNA replication and DNA damage repair pathways in esophageal cancer [19]. The MYC proto-oncogene encodes a DNA-binding factor that governs the transcriptional regulation of genetic information [20].…”

Section: Discussionmentioning

confidence: 99%

FAM111B knockdown attenuates tumorigenesis of ovarian cancer via the down regulation of MYC

Yu,

Wei,

et al. 2024

Preprint

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Background Ovarian cancer, a prevalent malignancy with the highest fatality rate among gynecological cancers, continues to face challenges in the development of effective targeted therapy approaches. While the FAM111B gene has been implicated in various cancer types, its specific role in ovarian cancer remains poorly understood. Methods The ES2 and A2780 ovarian cell lines were used to explore the cellular proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) in FAM111B knockdown experiments. The mouse tumor model was constructed to investigate the impact of FAM111B silencing in vivo. Tissue microarray was used to explore the prognostic value of different FAM111B expression level. Western blotting assay, MYC overexpression rescue experiments, protein transcriptomics and bioinformatics analysis were employed to explore the downstream molecular mechanism of FAM111B. Results The in vitro experiments indicated that the inhibition of FAM111B resulted in decreased cellular proliferation, migration, invasion, and EMT in ovarian cancer cell lines. The suppression of FAM111B resulted in the suppression of tumor growth in a mouse xenograft model. Immunohistochemistry analyses conducted on tissue-microarray samples obtained from patients with serous ovarian cancer indicated that elevated levels of FAM111B expression were associated with unfavorable prognostic outcomes. The silencing of FAM111B mechanistically suppressed MYC expression, with subsequent MYC overexpression reversing the phenotypic suppression caused by FAM111B silencing. Additionally, protein transcriptomics analysis indicated that FAM111B is implicated in genetic information processing via the MYC pathway, underscoring its central role in ovarian cancer tumorigenesis. Conclusions These findings suggest that FAM111B may serve as a novel biomarker and potential therapeutic target for ovarian cancer.

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Section: Discussionmentioning

confidence: 99%

FAM111B knockdown attenuates tumorigenesis of ovarian cancer via the down regulation of MYC

Yu,

Wei,

et al. 2024

Preprint

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“…Downregulation of GSDMA significantly enhances the proliferation and invasive potential of esophageal cancer cells, a phenomenon that is intricately linked to changes in cell sensitivity to cisplatin. 423 In individuals with HER2 + breast cancer, elevated levels of GSDMB correlate with reduced survival rates and an increased propensity for metastatic progression. 165,166 It is shown that upregulation of GSDMB can confer resistance to therapeutic interventions in HER2 + cancer cells through activation of the protective autophagy pathway, in which the interaction of GSDMB-NT with LC3B and Rab7 is critical for the activation of pro-survival autophagy.…”

Section: Cancersmentioning

confidence: 99%

The gasdermin family: emerging therapeutic targets in diseases

Zhu,

Xu,

Jiang

et al. 2024

Sig Transduct Target Ther

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The gasdermin (GSDM) family has garnered significant attention for its pivotal role in immunity and disease as a key player in pyroptosis. This recently characterized class of pore-forming effector proteins is pivotal in orchestrating processes such as membrane permeabilization, pyroptosis, and the follow-up inflammatory response, which are crucial self-defense mechanisms against irritants and infections. GSDMs have been implicated in a range of diseases including, but not limited to, sepsis, viral infections, and cancer, either through involvement in pyroptosis or independently of this process. The regulation of GSDM-mediated pyroptosis is gaining recognition as a promising therapeutic strategy for the treatment of various diseases. Current strategies for inhibiting GSDMD primarily involve binding to GSDMD, blocking GSDMD cleavage or inhibiting GSDMD-N-terminal (NT) oligomerization, albeit with some off-target effects. In this review, we delve into the cutting-edge understanding of the interplay between GSDMs and pyroptosis, elucidate the activation mechanisms of GSDMs, explore their associations with a range of diseases, and discuss recent advancements and potential strategies for developing GSDMD inhibitors.

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The role of pyroptosis in cancer: key components and therapeutic potential

Liu,

Xu,

Chen

et al. 2024

Cell Commun Signal

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Pyroptosis is a lytic and inflammatory form of gasdermin protein-mediated programmed cell death that is typically initiated by inflammasomes. The inflammasome response is an effective mechanism for eradicating germs and cancer cells in the event of cellular injury. The gasdermin family is responsible for initiating pyroptosis, a process in which holes are made in the cell membrane to allow inflammatory chemicals to escape. Mounting evidence indicates that pyroptosis is critical for controlling the development of cancer. In this review, we provide a general overview of pyroptosis, examine the relationship between the primary elements of pyroptosis and tumors, and stress the necessity of pyroptosis-targeted therapy in tumors. Furthermore, we explore its dual nature as a double-edged sword capable of both inhibiting and facilitating the growth of cancer, depending on the specific conditions. Ultimately, pyroptosis is a phenomenon that has both positive and negative effects on tumors. Using this dual impact in a reasonable manner may facilitate investigation into the initiation and progression of tumors and offer insights for the development of novel treatments centered on pyroptosis.

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Overexpressed FAM111B degrades GSDMA to promote esophageal cancer tumorigenesis and cisplatin resistance

Cited by 5 publications

References 38 publications

FAM111B knockdown attenuates tumorigenesis of ovarian cancer via the down regulation of MYC

FAM111B knockdown attenuates tumorigenesis of ovarian cancer via the down regulation of MYC

The gasdermin family: emerging therapeutic targets in diseases

The role of pyroptosis in cancer: key components and therapeutic potential

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