FSCN1 Promotes Esophageal Carcinoma Progression Through Downregulating PTK6 via its RNA-Binding Protein Effect

Cai, Hongfei; Wang, Rui; Tang, Ze; Lu, Tianyu; Cui, Youbin

doi:10.3389/fphar.2022.868296

Cited by 4 publications

(3 citation statements)

References 39 publications

(43 reference statements)

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“…In esophageal squamous cell carcinoma, FSCN1 was reported to promote tumor progression by the AKT/GSK3β signaling pathway [ 35 ]. Moreover, in lung adenocarcinoma, FSCN1 promotes tumor development through PI3K/AKT signaling [ 36 ].…”

Section: Discussionmentioning

confidence: 99%

FSCN1 promotes proliferation, invasion and glycolysis via the IRF4/AKT signaling pathway in oral squamous cell carcinoma

Chen

et al. 2023

BMC Oral Health

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Background Oral squamous cell carcinoma (OSCC) is a disease with increasing incidence worldwide that leads to deformity and death. In OSCC, fascin actin-bundling protein 1 (FSCN1) is an oncogene involved in the tumorigenesis process. However, the functions and potential mechanisms of FSCN1 in the OSCC tumorigenesis process have not been reported thus far. Methods We used qRT‒PCR to detect the expression of FSCN1 in 40 paired OSCC tumor tissues (tumor) and neighboring noncancerous tissues. The role of FSCN1 was also assessed in vitro through colony formation, CCK-8, and transwell assays. Moreover, glucose consumption was detected. Western blotting was used to confirm the interaction of FSCN1, IRF4 and AKT. Results FSCN1 was remarkably overexpressed in OSCC tissues and cell lines compared to corresponding controls. In addition, colony formation, CCK-8, and transwell assays revealed a notable reduction in OSCC growth and invasion when FSCN1 was silenced. FSCN1 silencing remarkably suppressed OSCC glycolysis. Mechanistic studies showed that FSCN1 achieves its function partially by activating interferon regulatory factor 4 (IRF4) and the AKT pathway in OSCC. Conclusion In conclusion, our study investigated the functions and mechanisms of the FSCN1/IRF4/AKT pathway in OSCC progression. In OSCC, FSCN1 is likely to be a biomarker and therapeutic target.

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Section: Discussionmentioning

confidence: 99%

FSCN1 promotes proliferation, invasion and glycolysis via the IRF4/AKT signaling pathway in oral squamous cell carcinoma

Chen

et al. 2023

BMC Oral Health

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“…In esophageal squamous cell carcinoma, FSCN1 was reported to promote tumor progression by AKT/GSK3β signaling pathway (35). Moreover, in lung adenocarcinoma, FSCN1 promoted tumor development through the PI3K/AKT signaling (36).…”

Section: Discussionmentioning

confidence: 99%

FSCN1 promotes proliferation, migration and glycolysis via the IRF4/AKT signalling pathway in oral squamous cell carcinoma

Chen

et al. 2022

Preprint

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Background: Oral squamous cell carcinoma (OSCC) is an increasing disease worldwide that leads to lethal and deforming consequences. In OSCC, Fascin actin-bundling protein 1 (FSCN1) is identified as an oncogene involved in the tumorigenesis process. But the functions as well as potential mechanisms of FSCN1 in OSCC tumorigenesis process have not been reported so far. Methods: We used RNA sequencing to detect the expreesion of FSCN1 from 40 paired OSCC tissue specimens (Tumor) and neighboring noncancerous tissue. Further colony formation, CCK-8 as well as transwell assay was performed to demonstrate the role of FSCN1 in vitro. Moreover, glucose consumption was detected. Western blot was used to confirm the interaction of FSCN1, IRF4 and AKT. Results: FSCN1 was remarkably overexpressed in OSCC cell lines as well as tissues. Further colony formation, CCK-8 as well as transwell assay suggested that FSCN1 silencing remarkably dampened OSCC growth and migration. Detection of glycolytic metabolism showed that FSCN1 silence remarkably suppressed OSCC glycolysis. Following mechanism studies revealed that FSCN1 realized its functions in OSCC process partially through the interferon regulatory factor 4 (IRF4) and AKT activation. Conclusion: In conclusion, our study investigated the functions as well as the mechanisms of the FSCN1/IRF4/AKT pathway in OSCC progression. FSCN1 could act as a prospective biologic signature and therapeutic target molecule for OSCC.

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“…RBPs regulate mRNA processing, transport, stability and translation, and are thus critical for various biological pathways as well as pathological changes, including cancer [7][8][9][10][11]. FSCN1 was rst identi ed as an RBP in HeLa cells [12], followed by esophageal cancer cells [13]. However, it is unclear whether it functions as an RBP in BLCA.…”

Section: Introductionmentioning

confidence: 99%

FSCN1/METTL3/TLN1 axis promotes the malignant progression in bladder carcinoma

Sun

Liu

Wang

et al. 2022

Preprint

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Background The RNA-binding protein (RBP) played an important role in tumors. FSCN1 functioned as an oncogene in bladder carcinoma (BLCA). FSCN1 has not been reported as an RBP in BLCA. The mechanism by which FSCN1 promoted BLCA invasion and metastasis has remained unclear. Methods The FSCN1-bound RNAs in BLCA cell lines were identified using RIP-sequencing. The regulatory relationship between FSCN1 and METTL3 or TLN1 was verified by RNA immunoprecipitation (RIP), RNA pulldown assay, co-immunoprecipitation (Co-IP), western blotting, quantitative real-time PCR (qRT-PCR) and immunofluorescence. The metastatic abilities of the BCLA cells were evaluated by in vitro wound healing and transwell assays, as well as in vivo models. Results TLN1 protein levels were higher in BLCA tissues compared to the paired para-tumor tissues, whereas its mRNA expression was lower in the tumors. Mechanistically, FSCN1 bound to and upregulated METTL3, which in turn repressed TLN1 mRNA expression through the latter’s 3'UTR. In addition, FSCN1 bound to the CDS region of TLN1 mRNA and promoted its translation. Knocking down FSCN1, METTL3 and TLN1 individually had an inhibitory effect on the proliferation, invasion, migration and metastasis of BLCA cells. Conclusions FSCN1 functions as an RBP to promote proliferation, invasion and migration of BLCA cells. The FSCN1/METTL3/TLN1 axis is a potential therapeutic target for BLCA.

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FSCN1 Promotes Esophageal Carcinoma Progression Through Downregulating PTK6 via its RNA-Binding Protein Effect

Cited by 4 publications

References 39 publications

FSCN1 promotes proliferation, invasion and glycolysis via the IRF4/AKT signaling pathway in oral squamous cell carcinoma

FSCN1 promotes proliferation, invasion and glycolysis via the IRF4/AKT signaling pathway in oral squamous cell carcinoma

FSCN1 promotes proliferation, migration and glycolysis via the IRF4/AKT signalling pathway in oral squamous cell carcinoma

FSCN1/METTL3/TLN1 axis promotes the malignant progression in bladder carcinoma

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