Up-regulation of TIF1γ by valproic acid inhibits the epithelial mesenchymal transition in prostate carcinoma through TGF-β/Smad signaling pathway

Qi, Guanghui; Yu, Jianguo; Zhao, Ying; Wang, Chunhui; Zhang, Hongge; Xia, Qinghua

doi:10.1016/j.ejphar.2019.172551

Cited by 16 publications

(9 citation statements)

References 50 publications

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“…Importantly, U87 MG cells placed onto CAM seem to undergo dramatic morphological changes upon the treatment with NaVP (Figure S1). We hypothesize that in GBM tumors, both Sema3C overexpression and NaVP treatment operate via the same epithelial-to-mesenchymal transition mechanism as was shown in other studies with prostate cancer [32,33]. When in combination, Sema3C and NaVP components seem to have a synergistic effect on tumor development.…”

Section: Discussionsupporting

confidence: 63%

The Anti-Tumorigenic Activity of Sema3C in the Chick Embryo Chorioallantoic Membrane Model

Valiulytė

Curkūnavičiūtė

Ribokaitė

et al. 2019

IJMS

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Sema3C protein, a member of the class 3 family of secreted semaphorins, play an important role in tumor development by regulating cell proliferation, migration, invasion, and angiogenesis processes. Depending on the type and malignancy grade of the tumor, Sema3C function remains controversial. In this study, we constructed a stably overexpressing Sema3C glioblastoma cell line U87 MG and tested it on the chicken embryo chorioallantoic membrane (CAM) model with the aim to reveal Sema3C protein function on angiogenesis process in ovo. Our experiments showed that Sema3C not only affects angiogenesis of CAM by inhibiting neovascularization but also acts as an anti-tumorigenic molecule by hampering U87 MG cell invasion into mesenchyme. The effects of Sema3C on CAM were similar to the effects of anti-epileptic drug sodium valproate (NaVP). Both, anti-angiogenic and anti-tumorigenic activities of Sema3C were enhanced by the treatment of NaVP and, importantly, were not attributed to the cytotoxic effects. Our studies suggest that Sema3C could be a promising target for glioblastoma treatment.

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Section: Discussionsupporting

confidence: 63%

The Anti-Tumorigenic Activity of Sema3C in the Chick Embryo Chorioallantoic Membrane Model

Valiulytė

Curkūnavičiūtė

Ribokaitė

et al. 2019

IJMS

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“…27 In vitro and in vivo studies have confirmed that TRIM33 plays an important role in valproic acid inhibiting the migration and invasion of prostate cancer cells. 28 This study also demonstrated that TRIM3 expression was decreased in TNF-α-induced MH7A cells and overexpression of TRIM3 suppressed the proliferation, invasion, and migration of TNF-α-induced MH7A cells.…”

Section: Discussionsupporting

confidence: 57%

KLF9 positively regulates TRIM33 to inhibit abnormal synovial fibroblast proliferation, migration as well as inflammation in rheumatoid arthritis

Dan

Tao

2022

Immunity Inflam & Disease

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Background Rheumatoid arthritis (RA) can cause irreversible joint injury and serious disability. This study aimed to investigate how TRIM33 regulated by KLF9 affects the aggressive behaviors of synovial fibroblasts induced by tumor necrosis factor‐α (TNF‐α). Materials and Methods TNF‐α‐induced MH7A cells were used to simulate the in vitro model of RA. TRIM33 and KLF9 expression in TNF‐α‐challenged MH7A cells and transfection efficiency were analyzed via real‐time reverse transcription polymerase chain reaction together with western blot. The viability, proliferation, invasion, and migration of TNF‐α‐induced MH7A cells after transfection was respectively detected by CCK‐8, EdU staining, transwell, and wound‐healing assays. The expression of invasion and migration‐related proteins and inflammation‐related proteins was determined by western blot and the levels of inflammatory factors were detected by enzyme‐linked immunosorbent assay. The combination between TRIM33 and KLF9 was substantiated through dual‐luciferase reporter assay and chromatin immunoprecipitation. Results TRIM33 and KLF9 expression in TNF‐α‐challenged MH7A cells was downregulated. TRIM33 elevation inhibited TNF‐α‐elicited proliferation, metastasis as well as inflammation of MH7A cells. Moreover, KLF9 was combined with TRIM33 and KLF9 promoted transcription of TRIM33. The inhibitory effect of TRIM33 overexpression on proliferation, invasion and migration and inflammation of MH7A cells induced by TNF‐α was alleviated by the downregulation of KLF9. Conclusion KLF9 positively regulates TRIM33 to suppress the abnormal MH7A cell proliferation, migration, and reduce inflammation upon exposure to TNF‐α, which was reversed by inhibiting KLF9.

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“…The TGF‐β/Smad signaling has been identified to play an essential part in various pathophysiologic processes, including cellular responses such as differentiation, proliferation, growth, migration, survival (Gao et al, 2019), and also be as a key driver of cancer progression, including PCa. For example, in PCa, valproic acid elevates the expression of transcriptional intermediary factor 1‐γ to suppress the EMT by regulating the TGF‐β/Smad signaling pathway (Qi et al, 2019). TGF‐β signaling accelerates the stemness of PCa cells by regulating the expression of SPOP (Jiao et al, 2020).…”

Section: Discussionmentioning

confidence: 99%

PAX3 silencing inhibits prostate cancer progression through the suppression of the TGF‐β/Smad signaling axis

Zeng

Xie

Huang

et al. 2020

Cell Biology International

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Multiple studies have confirmed the pro‐oncogenic effects of PAX3 in an array of cancers, but its role in prostate cancer (PCa) remains largely undefined. The aim of this study is to investigate the role of PAX3 in PCa. PAX3 expression was compared between PCa tumor tissue and nontumor tissues and PCa cell lines and normal prostate epithelial cells (PNT2) by western blot analysis and immunohistochemistry staining. MTT and immunofluorescence assays were used to detect PCa cell proliferation. Flow cytometry was used to evaluate cell apoptosis in PCa. Transwell assays were used for the determination of cell migration and PCa cell invasion. PAX3 expression was higher in PCa tissues and human PCa cell lines. Moreover, PAX3 silencing inhibited the proliferation, metastasis, and epithelial–mesenchymal transition (EMT) of PCa cells, and increased the rates of apoptosis. PAX3 silencing inhibited transforming growth factor‐β (TGF‐β)/Smad signaling in PCa cells. The effects of si‐PAX3 on the proliferation, apoptosis, metastasis, and EMT of PCa cells were alleviated by TGF‐β1 treatment. PAX3 silencing inhibits PCa progression through the inhibition of TGF‐β/Smad signaling. This reveals PAX3 as a novel biomarker and therapeutic target for future PCa treatments.

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Up-regulation of TIF1γ by valproic acid inhibits the epithelial mesenchymal transition in prostate carcinoma through TGF-β/Smad signaling pathway

Cited by 16 publications

References 50 publications

The Anti-Tumorigenic Activity of Sema3C in the Chick Embryo Chorioallantoic Membrane Model

The Anti-Tumorigenic Activity of Sema3C in the Chick Embryo Chorioallantoic Membrane Model

KLF9 positively regulates TRIM33 to inhibit abnormal synovial fibroblast proliferation, migration as well as inflammation in rheumatoid arthritis

PAX3 silencing inhibits prostate cancer progression through the suppression of the TGF‐β/Smad signaling axis

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