TGF-β1 induced fascin1 expression facilitates the migration and invasion of kidney carcinoma cells through ERK and JNK signaling pathways

Yang, Jianyu; Zhang, Naiwen; Gao, Ruxu; Zhu, Yuyan; Zhang, Zhe; Xu, Xiaolong; Wang, Jianfeng; Li, Zeliang; Liu, Xiankui; Li, Zhenhua; Li, Jun; Bi, Jianbin; Kong, Chuize

doi:10.1016/j.bbrc.2018.05.081

Cited by 20 publications

(12 citation statements)

References 29 publications

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“…For instance, UV radiation induces EMT-related molecules including Snail and Slug via the activation of ERK and p38 MAPK in keratinocytes [28]. Other evidence shows that TGF- β 1-induced fascin1 facilitates the migration and invasion of kidney carcinoma cells through ERK and JNK signaling pathways [29]. In this study, the overexpression of NQO1 decreased the level of phosphorylated AKT, JNK, and p38 MAPK, while knockdown increased their level.…”

Section: Discussionmentioning

confidence: 49%

Tumor Suppressive Function of NQO1 in Cutaneous Squamous Cell Carcinoma (SCC) Cells

Zhang

Lian

et al. 2019

BioMed Research International

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Cutaneous squamous cell carcinoma (SCC) is a common cancer that significantly decreases the quality of life. It is known that external stimulus such as ultraviolet (UV) radiation induces cutaneous SCC via provoking oxidative stress. NAD(P)H dehydrogenase 1 (NQO1) is a ubiquitous flavoenzyme that functions as a guardian against oxidative stress. However, the effect of NQO1 on cutaneous SCC is not clearly elucidated. In this study, we investigated the effect of NQO1 on cutaneous SCC cells using the recombinant adenoviruses that can upregulate and/or downregulate NQO1 expression. Overexpression of NQO1 resulted in significant decrease of cell proliferation and colony forming activity of SCC lines (SCC12 and SCC13 cells). By contrast, knockdown of NQO1 increased the cell proliferation and colony forming activity. Accordingly, the levels of proliferation-related regulators, such as Cyclin D1, Cyclin E, PCNA, SOX2, and p63, were decreased by the overexpression of NQO1, while those were increased by knockdown of NQO1. In addition, NQO1 affected the invasion and migration of SCC cells in a very similar way, with the regulation of epithelial-mesenchymal transition- (EMT-) related molecules, including E-cadherin, N-cadherin, Vimentin, Snail, and Slug. Finally, the overexpression of NQO1 decreased the level of phosphorylated AKT, JNK, and p38 MAPK, while the knockdown of NQO1 increased the level of phosphorylated signaling molecules. Based on these data, NQO1 has tumor suppressive function in cutaneous SCC cells.

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Section: Discussionmentioning

confidence: 49%

Tumor Suppressive Function of NQO1 in Cutaneous Squamous Cell Carcinoma (SCC) Cells

Zhang

Lian

et al. 2019

BioMed Research International

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“…TGF-β1 affects many biological processes [16] such as migration, invasion, and proliferation. In our previous studies, we found that TGF-β1 upregulated the expression of FSCN1 in BLCA [19] and KIRC [40]. Some studies have shown that TGF-β1 downregulates the expression of miR-200b [18, 41, 42].…”

Section: Discussionmentioning

confidence: 99%

“…Some studies have shown that TGF-β1 increases FSCN1 expression via the extracellular-signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) signaling pathways [40, 43]. Meanwhile, some studies reported that ZEB1-AS1 could affect cell function by regulating the Wnt/β-catenin [44] and p38MAPK signaling pathways, [45] which were also regulated by TGF-β1 [46–49].…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA ZEB1-AS1 regulates miR-200b/FSCN1 signaling and enhances migration and invasion induced by TGF-β1 in bladder cancer cells

Gao

Zhang

Yang

et al. 2019

J Exp Clin Cancer Res

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Background The effect of competing endogenous RNA (ceRNA) can regulate gene expression by competitively binding microRNAs. Fascin-1 (FSCN1) plays an important role in the regulation of cellular migration and invasion during tumor progression, but how its regulatory mechanism works through the ceRNA effect is still unclear in bladder cancer (BLCA). Methods The role of fascin-1, miR-200b , and ZEB1-AS1 in BLCA was investigated in vitro and in vivo. The interaction between fascin-1, miR-200b , and ZEB1-AS1 was identified using bioinformatics analysis, luciferase activity assays, RNA-binding protein immunoprecipitation (RIP), quantitative PCR, and western blotting. Loss (or gain)-of-function experiments were performed to investigate the biological roles of miR-200b and ZEB1-AS1 on migration, invasion, proliferation, cell apoptosis, and cell cycle. Results ZEB1-AS1 functions as a competing endogenous RNA in BLCA to regulate the expression of fascin-1 through miR-200b . Moreover, the oncogenic long non-coding RNA ZEB1-AS1 was highly expressed in BLCA and positively correlated with high tumor grade, high TNM stage, and reduced survival of patients with BLCA. Moreover, ZEB1-AS1 downregulated the expression of miR-200b , promoted migration, invasion, and proliferation, and inhibited apoptosis in BLCA. Furthermore, we found TGF-β1 induced migration and invasion in BLCA by regulating the ZEB1-AS1 / miR-200b /FSCN1 axis. Conclusion The observations in this study identify an important regulatory mechanism of fascin-1 in BLCA, and the TGF-β1/ ZEB1-AS1 / miR-200b /FSCN1 axis may serve as a potential target for cancer therapeutic purposes. Electronic supplementary material The online version of this article (10.1186/s13046-019-1102-6) contains supplementary material, which is available to authorized users.

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“…a previous study reported that the inhibition of FScn1 decreased the activity of the MaPK pathway and suppressed the growth and metastasis of non-small cell lung cancer (nSclc) cells, indicating that it may be a potentially effective therapeutic strategy for treating nSclc (28). in addition, FScn1 is an important mediator of TGF-β1-induced invasion and migration of kidney cancer cells (KCC) via ERK and JNK signaling pathways (29). FScn1 could act as an oncogene and a potential novel prognostic biomarker for patients with renal cell carcinoma (rcc) after nephrectomy, and can promote rcc metastasis (30).…”

Section: Fscn1 Is Overexpressed and Stimulates The Metastasis Of CCmentioning

confidence: 98%

MicroRNA‑145‑5p suppresses fascin to inhibit the invasion and migration of cervical carcinoma cells

Peng

et al. 2020

Mol Med Rep

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Micrornas (mirs) can affect the progression of cervical cancer (cc). The present study investigated the function of mir-145-5p in cc and demonstrated its association with fascin (FScn1). The expression levels of mir-145-5p in cc tissues and cell lines were analyzed using reverse transcription-quantitative Pcr, and its direct targets were explored using a luciferase reporter assay. The viability, migration and invasion of Hela cells transfected with small interfering FScn1 or with mir-145-5p mimics and inhibitors were analyzed using cell counting Kit-8 and Transwell assays. The expression levels of FScn1 mrna and protein were investigated using reverse transcription Pcr and western blotting. mir-145-5p was downregulated in cc tissues and cell lines. Moreover, overexpression of mir-145-5p inhibited the migration, invasion and viability of Hela cells. mir-145-5p directly targeted FScn1, which regulated the suppressive functions of mir-145-5p in cc cells. overall, mir-145-5p is a tumor suppressor gene and a promising target for cc treatment.

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TGF-β1 induced fascin1 expression facilitates the migration and invasion of kidney carcinoma cells through ERK and JNK signaling pathways

Cited by 20 publications

References 29 publications

Tumor Suppressive Function of NQO1 in Cutaneous Squamous Cell Carcinoma (SCC) Cells

Tumor Suppressive Function of NQO1 in Cutaneous Squamous Cell Carcinoma (SCC) Cells

Long non-coding RNA ZEB1-AS1 regulates miR-200b/FSCN1 signaling and enhances migration and invasion induced by TGF-β1 in bladder cancer cells

MicroRNA‑145‑5p suppresses fascin to inhibit the invasion and migration of cervical carcinoma cells

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