&lt;p&gt;LukS-PV Inhibits Hepatocellular Carcinoma Cells Migration via the TNNC1/PI3K/AKT Axis&lt;/p&gt;

Wang, Ziran; Qiang, Ya‐Wei; Xu, Lei; Ding, Pengsheng; Wang, Yangyan; Ma, Xiaoling

doi:10.2147/ott.s278540

Cited by 8 publications

(3 citation statements)

References 31 publications

(39 reference statements)

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“…Besides, high level of TNNC1 was found to be associated with poor prognosis of patients with gastric cancer. The highly expressed TNNC1 was previously identified in hepatocellular carcinoma cells [16], and tongue squamous cell carcinoma tissues [30]. These previous data together with ours suggested the potential of TNNC1 as a biomarker of cancer diagnosis and prognosis.…”

Section: Discussionsupporting

confidence: 83%

Troponin C-1 Activated by E2F1 Accelerates Gastric Cancer Progression via Regulating TGF-β/Smad Signaling

Fang

Zhang

et al. 2021

Dig Dis Sci

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Background Troponin C-1 (TNNC1) has been previously characterized as an oncogenic gene. Aims This study aimed to reveal the roles of TNNC1 in gastric cancer and the potential underlying mechanisms. Methods TNNC1 siRNAs and TNNC1 overexpression plasmid were used to alter its expression in AGS, MKN45, and HGC-27 cells. CCK-8 assay, colony formation, EdU assay, flow cytometry, transwell assay, and scratch test were conducted to measure the phenotype changes. In vivo effects of TNNC1 silence were confirmed by using a xenograft mouse model. Bioinformatics analysis was conducted to screen out the transcription factor and downstream signaling of TNNC1. Results TNNC1 was highly expressed in gastric cancer tissues and cell lines, and its expression was associated with poor prognosis. TNNC1 silence suppressed the proliferation, migration, and invasion of AGS and MKN45 cells. However, TNNC1 silence induced apoptosis by mediating the cleavage of caspase-3 and caspase-9. Overexpression of TNNC1 in HGC-27 cells led to the contrary effects. The anti-tumor effects of TNNC1 silence were also confirmed in a xenograft animal model. E2F1 was validated as an upstream transcription factor of TNNC1. Effects of TNNC1 silence on AGS cell migration and invasion were attenuated by E2F1 overexpression. Besides, TGF-β/Smad was a downstream signaling pathway of TNNC1. The anti-tumor impacts of TNNC1 silence were weaken by SB431542 (a specific inhibitor of TGF-β signaling) while accelerated by TGF-β. Conclusion TNNC1 activated by E2F1 functioned as an oncogenic gene through regulating TGF-β/Smad signaling. TNNC1 was suggested as a potential molecular drug target of gastric cancer.

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Section: Discussionsupporting

confidence: 83%

Troponin C-1 Activated by E2F1 Accelerates Gastric Cancer Progression via Regulating TGF-β/Smad Signaling

Fang

Zhang

et al. 2021

Dig Dis Sci

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“…Our previous study demonstrated that LukS-PV inhibited HCC cell migration by interfering with PI3K-AKT signaling [ 26 ]. However, it remains unknown whether LukS-PV can inhibit HCC cell migration through acetylation pathways.…”

Section: Introductionmentioning

confidence: 99%

LukS-PV inhibits hepatocellular carcinoma cells migration by downregulating HDAC6 expression

Ding

Shi

et al. 2022

BMC Cancer

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Background Hepatocellular carcinoma (HCC) is a clinically common malignant tumor worldwide. LukS-PV is the S component of Panton-Valentine leukocidin secreted by Staphylococcus aureus, which has shown anti-cancer activity. Based on previous findings, this study investigated the effects of LukS-PV on HCC migration and the potential molecular mechanisms involving acetylation pathways. Methods After treating HCC cells with different concentrations of LukS-PV, we used scratch assays to determine the mobility of the cancer cells. Western blots were used to determine the expression levels of migration-related proteins. Quantitative proteomic sequencing was used to evaluate proteomic changes in target proteins. Immunoprecipitation and liquid chromatography coupled with tandem mass spectrometry analyses were used to validate the binding of related target proteins. Results LukS-PV inhibited HCC cell migration in a concentration-dependent manner. In addition, LukS-PV attenuated the expression of histone deacetylase (HDAC)6, which is highly expressed in HCC cells. Further studies showed that LukS-PV increased the acetylation level of α-tubulin by down-regulating HDAC6, which resulted in the inhibition of HCC cell migration. Conclusion Taken together, our data revealed a vital role of LukS-PV in suppressing HCC cell migration by down-regulating HDAC6 and increasing the acetylation level of α-tubulin.

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“…TFAP4 activates the PI3K/AKT signal pathway, hence boosting tumor invasion and metastasis in liver cancer [ 15 ]. PI3K/AKT pathway inhibition exerts an antitumor function in HCC [ 16–18 ]. Nonetheless, whether the TFAP4/PI3K/AKT axis takes part in HCC development remains poorly understood.…”

Section: Introductionmentioning

confidence: 99%

Upregulating microRNA-373-3p promotes apoptosis and inhibits metastasis of hepatocellular carcinoma cells

Wang

et al. 2022

Bioengineered

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Hepatocellular carcinoma (HCC) is one of the most prevalent malignancies in the digestive system. Abnormal miR-373-3p and TFAP4 expressions are critical in many malignant tumors, but it is unclear whether they work in the context of HCC. qRT-PCR measured miR-373-3p expression in HCC tissues and adjacent normal tissues. Flow cytometry and Western blot analyzed cell apoptosis. EMT, Transwell, and wound healing assay examined HCC cell migration and EMT, respectively. Western blot determined the profile of TFAP4/PI3K/AKT. IHC detected Ki67, E-cadherin, and vimentin in the tumor tissues. Moreover, the downstream target of miR-373-3p was predicted using the database. Dual luciferase activity assay and RIP verified the binding correlation between TFAP4 and miR-373-3p. In HCC tissues and cell lines, miR-373-3p was downregulated, and its overexpression stepped up HCC cell apoptosis and suppressed migration and EMT. Furthermore, miR-373-3p overexpression elevated Bax and caspase 3 expressions and attenuated Bcl2’s level. A xenograft tumor experiment in nude mice unveiled that miR-373-3p overexpression dampened tumor growth and proliferation. miR-373-3p cramped PI3K/AKT pathway activation. miR-373-3p negatively modulated TFAP4, and TFAP4 overexpression inverted miR-373-3p-mediated anti-tumor effects. Additionally, TFAP4 enhanced IGF1 expression, and promoted IGF1R-PI3K/AKT pathway activation. Collectively, miR-373-3p functions as an anti-tumor gene in HCC by inhibiting TFAP4/PI3K/AKT pathway.

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<p>LukS-PV Inhibits Hepatocellular Carcinoma Cells Migration via the TNNC1/PI3K/AKT Axis</p>

Cited by 8 publications

References 31 publications

Troponin C-1 Activated by E2F1 Accelerates Gastric Cancer Progression via Regulating TGF-β/Smad Signaling

Troponin C-1 Activated by E2F1 Accelerates Gastric Cancer Progression via Regulating TGF-β/Smad Signaling

LukS-PV inhibits hepatocellular carcinoma cells migration by downregulating HDAC6 expression

Upregulating microRNA-373-3p promotes apoptosis and inhibits metastasis of hepatocellular carcinoma cells

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