Calycosin inhibits breast cancer cell migration and invasion by suppressing EMT via BATF/TGF-β1

Zhang, Zhenxia; Lin, Min; Wang, Junli; Yang, Fenglian; Peng, Yang; Liu, Yaqun; Chen, Zikai; Zheng, Yuzhong

doi:10.18632/aging.203093

Cited by 41 publications

(27 citation statements)

References 36 publications

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“…In this study, it was demonstrated that calycosin could inhibit the proliferation, migration, invasion, and EMT progression of LUAD cells (A549, H1299) in a dose-dependent manner. These were generally consistent with the findings of Zhang et al in breast cancer cells [ 20 ], indicating that calycosin could exert an inhibitory role in the progression of LUAD.…”

Section: Discussionsupporting

confidence: 92%

Calycosin Inhibits the Malignant Behaviors of Lung Adenocarcinoma Cells by Regulating the circ_0001946/miR-21/GPD1L/HIF-1α Signaling Axis

et al. 2022

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Objective. To clarify the potential function and molecular mechanism of calycosin in lung adenocarcinoma (LUAD) cells. Methods. LUAD cells (A549 and H1299) were treated with calycosin at different concentrations (25 nM, 50 nM, and 100 nM) for 24 h. The colony formation, invasion, and migration of the cells were assessed by colony formation, transwell, and scratch assays, respectively. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was performed to determine the mRNA expression level of circ_0001946, miR-21, glycerol-3-phosphate dehydrogenase 1 like (GPD1L), and hypoxia-inducible factor-1α (HIF-1α) in clinical tissue samples and LUAD cells. RNA pull-down assay and dual-luciferase reporter assay were performed to verify the relationship among circ_0001946, miR-21, GPD1L, and HIF-1α. Western blot was performed to detect the protein expression of epithelial-mesenchymal transition (EMT) process-related genes (E-cadherin, N-cadherin, and snail) and GPD1L as well as HIF-1α. Results. Calycosin inhibited colony formation, invasion, migration, and EMT progression in A549 and H1299 cells. Besides, calycosin was able to regulate the expression of circ_0001946, miR-21, GPD1L, and HIF-1α in LUAD cells. According to the findings of QRT-PCR, the expression level of circ_0001946 and GPD1L in LUAD tissues was significantly lower than that in adjacent noncancerous normal tissues, and the expression of miR-21 and HIF-1α was also significantly increased in clinical tissue samples. In addition, there was a targeted regulatory relationship among the above four expressions. Knockdown of circ_0001946 expression in A549 cells treated with calycosin enhanced the malignant behavior of A549 cells and inhibited the anticancer effect of calycosin. However, the knockdown of miR-21 promoted the anticancer effect of calycosin and inhibited the malignant behavior of A549. Conclusion. Calycosin can inhibit colony formation, invasion, migration, and EMT process of LUAD cells via regulating the circ_0001946/miR-21/GPD1L/HIF-1α signaling axis and could be a promising therapeutic drug for LUAD.

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Section: Discussionsupporting

confidence: 92%

Calycosin Inhibits the Malignant Behaviors of Lung Adenocarcinoma Cells by Regulating the circ_0001946/miR-21/GPD1L/HIF-1α Signaling Axis

et al. 2022

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“…Similar results were reported by Hao Huang[15], who demonstrated that BATF was identi ed as a better prognostic model from 143 methylation-driven genes in Colorectal Carcinoma. While the previous an inconsistent study showed that BATF promoted breast cancer cell migration and invasiveness by increasing TGFβ1 mRNA and protein levels [16]. Collectively these studies failed to reach a consistent conclusion and in ccRCC the prognostic inconsistency of BATF may be due to the heterogeneity of ccRCC specimens.…”

Section: Discussionmentioning

confidence: 91%

BATF Inhibits Cell Proliferation and Migration via PI3K/AKT/mTOR Pathway in Clear Cell Renal Cell Carcinoma

Li¹,

Jin²,

Yang³

et al. 2021

Preprint

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Background Previous studies reported that BATF played an important role in the progression of various cancers, but no report had been found on clear cell renal cell carcinoma(ccRCC). So we investigated the effects of BATF on the progression of ccRCC. Methods In this study, using TCGA-KIRC database from the Cancer Genome Atlas to analyze the differential genes of BATF in ccRCC ; using immunohistochemistry to detect BATF expression in 75 ccRCC tumorous and 28 nontumorous tissues, and investigate its relationship with clinicopathological parameters. Moreover, we constructed the cell lines of BATF overexpression and knockout in Caki-1and 786-0 ccRCC cell lines and confirmed by western blot. CCK8 assay was used to evaluated the cell viability and using EdU staining to detect cell proliferation; using Transwell experiment to investigate the affection of BATF in ccRCC cell migration. Westernblot was used to detect the phosphorylation of PI3K/AKT/mTOR. Results These results revealed that BATF expression in ccRCC tumorous was significantly higher compared with that in adjacent nontumorous tissues and was significantly correlated with T stage, Fuhrman grade, Tumor necrosis and status. In addiditon, BATF overexpression significantly inhibited the viability, proliferation and migration of the two cell lines. More importantly, using westernblot showed that silencing BATF significantly increased the level of phosphorylated AKT, PI3K and mTOR, while BATF overexpression decreased phosphorylation that involved in the PI3K/Akt/mTOR signaling pathway. Conclusions Our findings demonstrate that BATF plays an important role in the progression of ccRCC and it may act as an tumor supressor gene to inhibit the progression of ccRCC through regulating the PI3K/Akt/mTOR signaling pathway.

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“…Meanwhile, it controls EMT-related and autophagy-related pathways such as PI3K/AKT, Wnt/β-catenin and MAPK/ERK signaling pathways [ 74 ]. Calycosin inhibits proliferation, migration and invasion of breast cancer cells in a time and dose-dependent manner, and also suppresses the progression of EMT [ 75 ]. Ononin has an anti-inflammatory effect on lipopolysaccharide (LPS)-induced inflammation [ 76 ], and reported to inhibit proliferation of breast cancer cells via PI3K/AKT/mTOR signaling pathway [ 77 ].…”

Section: Discussionmentioning

confidence: 99%

Astragalus mongholicus Bunge and Curcuma aromatica Salisb. inhibits liver metastasis of colon cancer by regulating EMT via the CXCL8/CXCR2 axis and PI3K/AKT/mTOR signaling pathway

et al. 2022

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Background One of the most challenging aspects of colon cancer (CC) prognosis and treatment is liver-tropic metastasis. Astragalus mongholicus Bunge—Curcuma aromatica Salisb. (AC) is a typical medication combination for the therapy of many malignancies. Our previous studies found that AC intervention inhibits liver metastasis of colon cancer (LMCC). Nevertheless, the comprehensive anti-metastasis mechanisms of AC have not been uncovered. Methods In bioinformatics analysis, RNA-seq data of CC and LMCC patients were collected from TCGA and GEO databases, and differentially expressed genes (DEGs) were identified. The biological processes and signaling pathways involved in DEGs were enriched by GO and KEGG. The protein–protein interaction (PPI) network of DEGs was established and visualized using the Cytocape software, followed by screening Hub genes in the PPI network using Degree value as the criterion. Subsequently, the expression and survival relevance of Hub gene in COAD patients were verified. In the experimental study, the effects of AC on the inhibition of colon cancer growth and liver metastasis were comprehensively evaluated by cellular and animal models. Finally, based on the results of bioinformatics analysis, the possible mechanisms of AC inhibition of colon cancer EMT and liver metastasis were explored by in vivo and in vitro pharmacological experiments. Results In this study, we obtained 2386 DEGs relevant to LMCC from the COAD (colon adenocarcinoma) and GSE38174 datasets. Results of GO gene function and KEGG signaling pathway enrichment analysis suggested that cellular EMT (Epithelial-mesenchymal transition) biological processes, Cytokine-cytokine receptor interaction and PI3K/Akt signaling pathways might be closely related to LMCC mechanism. We then screened for CXCL8, the core hub gene with the highest centrality within the PPI network of DEGs, and discovered that CXCL8 expression was negatively correlated with the prognosis of COAD patients. In vitro and in vivo experimental evidence presented that AC significantly inhibited colon cancer cell proliferation, migration and invasion ability, and suppressed tumor growth and liver metastasis in colon cancer orthotopic transplantation mice models. Concomitantly, AC significantly reduced CXCL8 expression levels in cell supernatants and serum. Moreover, AC reduced the expression and transcription of genes related to the PI3K/AKT pathway while suppressing the EMT process in colon cancer cells and model mice. Conclusions In summary, our research predicted the potential targets and pathways of LMCC, and experimentally demonstrated that AC might inhibit the growth and liver metastasis in colon cancer by regulating EMT via the CXCL8/CXCR2 axis and PI3K/AKT/mTOR signaling pathway, which may facilitate the discovery of mechanisms and new therapeutic strategies for LMCC.

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Calycosin inhibits breast cancer cell migration and invasion by suppressing EMT via BATF/TGF-β1

Cited by 41 publications

References 36 publications

Calycosin Inhibits the Malignant Behaviors of Lung Adenocarcinoma Cells by Regulating the circ_0001946/miR-21/GPD1L/HIF-1α Signaling Axis

Calycosin Inhibits the Malignant Behaviors of Lung Adenocarcinoma Cells by Regulating the circ_0001946/miR-21/GPD1L/HIF-1α Signaling Axis

BATF Inhibits Cell Proliferation and Migration via PI3K/AKT/mTOR Pathway in Clear Cell Renal Cell Carcinoma

Astragalus mongholicus Bunge and Curcuma aromatica Salisb. inhibits liver metastasis of colon cancer by regulating EMT via the CXCL8/CXCR2 axis and PI3K/AKT/mTOR signaling pathway

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