Scutellarin Inhibits Proliferation, Invasion, and Tumorigenicity in Human Breast Cancer Cells by Regulating HIPPO-YAP Signaling Pathway

Hou, Lengchen; Chen, Lei; Fang, Lin

doi:10.12659/msm.904492

Cited by 48 publications

(32 citation statements)

References 19 publications

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“…Substantial evidence has confirmed that SCU, a flavonoid isolated from Erigeron breviscapus (Vant.) Hand.‐Mazz., has antitumor effects on several cancers, including liver, colorectal, breast, and prostate, as well as lymphomas . However, little is known about its antitumor mechanisms and whether SCU can inhibit NSCLC when used alone.…”

Section: Introductionmentioning

confidence: 99%

“…Hand.-Mazz., has antitumor effects on several cancers, including liver, colorectal, breast, and prostate, as well as lymphomas. [15][16][17][18][19] However, little is known about its antitumor mechanisms and whether SCU can inhibit NSCLC when used alone. In the present study, we explored the effects of different concentrations of SCU on proliferation, apoptosis, and tumorigenesis, and the expression of AKT/mTOR/4E-BP1 and STAT3 signaling pathway proteins in cultured A549 lung cancer cells.…”

Section: Introductionmentioning

confidence: 99%

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Scutellarin suppresses proliferation and promotes apoptosis in A549 lung adenocarcinoma cells via AKT/mTOR/4EBP1 and STAT3 pathways

Cao

Liu

et al. 2019

Thoracic Cancer

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Background Scutellarin (SCU), a flavonoid isolated from Erigeron breviscapus (Vant.) Hand.‐Mazz., increases autophagy and apoptosis in the adenocarcinoma A549 cell line, which is resistant to cisplatin. However, whether SCU alone has antitumor activity against non‐small cell lung cancer (NSCLC) is unknown. Methods Cell Counting Kit‐8, flow cytometry, colony formation, Hoechst 33258 staining, and Western blot analyses were used to examine the proliferation and apoptosis of A549 cells treated with SCU and the possible molecular mechanisms. Results The cell viability assay indicated that SCU markedly suppressed the proliferation of A549 cells in concentration and time‐dependent manners. SCU caused significant G0/G1 phase arrest and apoptosis, as evidenced by flow cytometric analyses, Hoechst 33258 staining, and Western blot analyses of cyclin D1, cyclin E, BCL‐2, cleaved‐caspase‐3, and BAX. Furthermore, SCU treatment reduced the level of pan‐AKT, phosphorylated (p)‐mTOR, mTOR, BCL‐XL, STAT3, and p‐STAT3, and increased the level of 4EBP1. Conclusions SCU can suppress proliferation and promote apoptosis in A549 cells through AKT/mTOR/4EBP1 and STAT3 pathways. This suggests that SCU may be developed into a promising antitumor agent for treating NSCLC.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Scutellarin suppresses proliferation and promotes apoptosis in A549 lung adenocarcinoma cells via AKT/mTOR/4EBP1 and STAT3 pathways

Cao

Liu

et al. 2019

Thoracic Cancer

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“…LncRNA TNRC6C‐AS1 promoted STK4 by inhibiting the methylation of STK4 promoter, thus inhibiting the phosphorylation level of YAP and Hippo signalling pathway. Hippo signalling pathway is a development control signal pathway, which plays a regulatory role in cell proliferation and apoptosis . YAP is considered as the main effector of the Hippo signalling pathway in various organisms and tissues .…”

Section: Discussionmentioning

confidence: 99%

“…Hippo signalling pathway is a development control signal pathway, which plays a regulatory role in cell proliferation and apoptosis. 24 YAP is considered as the main effector of the Hippo signalling pathway in various organisms and tissues. 25 Knockdown of lncRNA GHET1 suppresses the cell proliferation and invasion by down-regulating YAP1 expression in the non-small cell lung cancer.…”

Section: Discussionmentioning

confidence: 99%

Long non‐coding RNA TNRC6C‐AS1 promotes methylation of STK4 to inhibit thyroid carcinoma cell apoptosis and autophagy via Hippo signalling pathway

Peng

Tan

et al. 2019

J Cellular Molecular Medi

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The role of long non‐coding RNAs (lncRNAs) in thyroid carcinoma (TC), the most frequent endocrine malignancy, has been extensively examined. This study investigated effect of interaction among lncRNA TNRC6C‐AS1, serine/threonine‐protein kinase 4 (STK4) and Hippo signalling pathway on TC. Initially, lncRNA TNRC6C‐AS1 expression in TC tissues was detected. To explore roles of lncRNA TNRC6C‐AS1, STK4 and Hippo signalling pathway in TC progression, their expressions were altered. Interaction between lncRNA TNRC6C‐AS1 and STK4, STK4 promoter methylation, or Hippo signalling pathway was verified. After that, a series of experiments were employed to evaluate in vitro ability of apoptosis, proliferation and autophagy of TC cells and in vivo tumorigenicity, and tumour growth of TC cells. lncRNA TNRC6C‐AS1 was highly expressed while STK4 was poorly expressed in TC tissues. LncRNA TNRC6C‐AS1 promoted the STK4 methylation and down‐regulated STK4 expression, which further activated the Hippo signalling pathway. STK4 silencing was observed to promote the proliferation ability of TC cells, inhibit the apoptosis and autophagy abilities, as well as enhance the tumorigenicity and tumour growth. Moreover, the in vitro proliferation ability as well as the in vivo tumorigenicity and tumour growth of TC cells were inhibited after the blockade of Hippo signalling pathway, while the apoptosis and autophagy abilities were promoted. The results demonstrate that the lncRNA TNRC6C‐AS1 increases STK4 promoter methylation to down‐regulate STK4 expression, thereby promoting the development of TC through activation of Hippo signalling pathway. It highlights that lncRNA TNRC6C‐AS1 may be a novel therapeutic target for the treatment of TC.

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“…JAG1 is a key ligand of the Notch pathway, implicated in tumorigenesis and vascularization (28)(29)(30). YAP1 has been demonstrated to regulate oncogenic phenotypes of breast cancer cells (31)(32)(33)(34), and JAG1 is associated with recurrence and poor prognosis in patients with breast cancer (35)(36)(37). Interestingly, it has previously been shown that YAP1 acts upstream of the Notch pathway and upregulates JAG1 expression (20,25,38).…”

Section: Linc-oip5 Loss Regulates Migration and Invasion In Mda-mb-231mentioning

confidence: 99%

Linc‑OIP5 loss regulates migration and invasion in MDA‑MB‑231 breast cancer cells by inhibiting YAP1/JAG1 signaling

Zhu

Dong

et al. 2019

Oncol Lett

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Breast cancer is the most prevalent cancer among women, and diagnosis and treatment represent a substantial challenge due to the lack of adequate molecular targets. It has been shown that long noncoding RNAs (lncRNAs) serve pivotal roles in regulating gene expression in tumors. The roles of long intervening noncoding RNA (Linc)-OIP5 has been demonstrated in different types of cancer; however, its function in breast cancer has not been determined. In the present study, expression of Linc-OIP5, YAP1 (Hippo signaling component) and JAG1 (Notch signaling component) in breast cancer cells with different degrees of malignancy were determined. To assess whether Linc-OIP5 regulated the malignant biological behaviors of MDA-MB-231 cells, its expression was knocked down using a specific small interfering RNA (siRNA), and cell proliferation was determined using a CCK-8 assay, apoptosis was evaluated using an Annexin V-FITC apoptosis detection kit, migration was assessed using a wound healing and transwell migration assays, and cell invasion examined using a transwell invasion assays. The effect of Linc-OIP5 knockdown on YAP1 and JAG1 expression was quantified using reverse transcription-quantitative PCR and immunoblotting. Cell proliferation, migration and invasion were reduced, while apoptosis was increased in MDA-MB-231 cells transfected with Linc-OIP5-specific siRNA. Mechanistic investigations showed that Linc-OIP5 knockdown downregulated YAP1 and JAG1 expression. The results of the present study suggest that Linc-OIP5 affects the malignant biological behaviors of MDA-MB-231 cells, at least partly through its effects on YAP1/JAG1 signaling. Whilst there are a number of mechanisms underlying the pathogenesis of breast cancer, the results of the present study highlight Linc-OIP5 as a potential therapeutic target in breast cancer.

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Scutellarin Inhibits Proliferation, Invasion, and Tumorigenicity in Human Breast Cancer Cells by Regulating HIPPO-YAP Signaling Pathway

Cited by 48 publications

References 19 publications

Scutellarin suppresses proliferation and promotes apoptosis in A549 lung adenocarcinoma cells via AKT/mTOR/4EBP1 and STAT3 pathways

Scutellarin suppresses proliferation and promotes apoptosis in A549 lung adenocarcinoma cells via AKT/mTOR/4EBP1 and STAT3 pathways

Long non‐coding RNA TNRC6C‐AS1 promotes methylation of STK4 to inhibit thyroid carcinoma cell apoptosis and autophagy via Hippo signalling pathway

Linc‑OIP5 loss regulates migration and invasion in MDA‑MB‑231 breast cancer cells by inhibiting YAP1/JAG1 signaling

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