RhBMP-2 Activates Hippo Signaling through RASSF1 in Esophageal Cancer Cells

Kim, Soo Mi; Ye, Shuai; Rah, So-Young; Park, Byung Hyun; Wang, Hong‐En; Kim, Jung-Ryul; Kim, Seung Ho; Jang, Kyu Yun; Lee, Kwang-Bok

doi:10.1038/srep26821

Cited by 11 publications

(11 citation statements)

References 36 publications

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“…These previous results are conspicuously consistent with our present results. Our current study surprisingly showed that complex formation via disruption of AKT-RASSF1 interaction [41]. Another report showed that canonical BMP signaling induces expression of RUNX3 and BMP2/4-induced RUNX3 suppress tumor growth through repression of c-Myc promoter activity via binging RUNXbinding elements in c-Myc promoter [25].…”

Section: Discussionsupporting

confidence: 51%

TrkB induced metastatic potential of cancer by suppression of BMP mediated tumor inhibitory activity

Kim¹,

Jin

2020

Preprint

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Our previous observations also demonstrate that TrkB expression in breast cancer induces metastatic potential by both JAK2/STAT3 and PI3K/AKT activation and induced metastasis of breast cancer mediated suppression of RUNX3 and KEAP1 expression by TrkB. Also, TrkB induced metastatic potential of cancer and suppressed the growth inhibitory activity in response to BMP signaling by preventing BMRRI/BMPRII complex formation. The previous report BMP-2 and BMP4 trigger tumor inhibitory activity in colorectal cancer by upregulation of RUNX3 expression. Although TrkB may regulate tumor inhibitory activity by BMP-induced upregulation of RUNX3, it is not still fully understood how TrkB signaling adjusts to inhibit BMP signaling-mediated tumor suppression.Our findings provide important molecular insights into TrkB-mediated modulation of BMP signaling has remained unknown, and none of the studies still reported a correlation between TrkB and BMP signaling. Our current study surprisingly showed that unique role of TrkB in the regulation of BMP-induced tumor inhibitory activity and BMP-2-induced RUNX3 expression.

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Section: Discussionsupporting

confidence: 51%

TrkB induced metastatic potential of cancer by suppression of BMP mediated tumor inhibitory activity

Kim¹,

Jin

2020

Preprint

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“…TAZ/YAP was also demonstrated to regulate BMP4 expression in zebrafish [69], and indirectly crosstalk with BMP2 signaling pathway [70]. Additionally, BMP2 has been suggested to induce cytoplasmic retention of YAP [71]. Thus, increasing data suggest crosstalk between BMPR and Hippo signaling pathways.…”

Section: Discussionmentioning

confidence: 96%

BMP6/TAZ-Hippo signaling modulates angiogenesis and endothelial cell response to VEGF

et al. 2020

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The BMP/TGFβ-Smad, Notch and VEGF signaling guides formation of endothelial tip and stalk cells. However, the crosstalk of bone morphogenetic proteins (BMPs) and vascular endothelial growth factor receptor 2 (VEGFR2) signaling has remained largely unknown. We demonstrate that BMP family members regulate VEGFR2 and Notch signaling, and act via TAZ-Hippo signaling pathway. BMPs were found to be regulated after VEGF gene transfer in C57/Bl6 mice and in a porcine myocardial ischemia model. BMPs 2/4/6 were identified as endothelium-specific targets of VEGF. BMP2 modulated VEGF-mediated endothelial sprouting via Delta like Canonical Notch Ligand 4 (DLL4). BMP6 modulated VEGF signaling by regulating VEGFR2 expression and acted via Hippo signaling effector TAZ, known to regulate cell survival/proliferation, and to be dysregulated in cancer. In a matrigel plug assay in nude mice BMP6 was further demonstrated to induce angiogenesis. BMP6 is the first member of BMP family found to directly regulate both Hippo signaling and neovessel formation. It may thus serve as a target in pro/anti-angiogenic therapies.

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“…Interestingly, MST1 could negatively regulated Akt activity and thereby promote GSK3β [25, 26], which could activate p21 [27]. So, the repression of p21 after KCTD11 knock-down in Huh7 could be a result of up-regulated MST1/GSK3β.…”

Section: Resultsmentioning

confidence: 99%

KCTD11 inhibits growth and metastasis of hepatocellular carcinoma through activating Hippo signaling

et al. 2017

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A lack of effective prognostic biomarkers and molecular targets is a serious problem in hepatocellular carcinoma. KCTD11, reported as a tumor suppressor, are still not well understood. In this study, KCTD11 was found low-expressed in HCC tissues and cell lines. The HCC patients with low expression of KCTD11 suggested shorter overall survival. We found KCTD11 inhibiting cell proliferation in vitro and tumor growth in vivo, by activating p21 and repressing cycle related proteins. KCTD11 also inhibited cell adhesion by decreasing CTGF and CLDN1. We found CTGF binding COL3A1 in HCCLM3, which might lead to reduction of COL3A1 expression. KCTD11 also inhibited cell migration and invasion in HCC, by repressing MMPs and EMT. We found the tumor suppression function of KCTD11 was at least partly through activating Hippo pathway in HCC. Base on the enhanced Hippo pathway, KCTD11 could activate p21 by stabilizing p53 or promoting the MST1/ GSK3β/p21 signaling in HCC. Overall, these results suggest that KCTD11 works as a tumor suppressor and owns prognostic and therapeutic potentials in HCC.

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RhBMP-2 Activates Hippo Signaling through RASSF1 in Esophageal Cancer Cells

Cited by 11 publications

References 36 publications

TrkB induced metastatic potential of cancer by suppression of BMP mediated tumor inhibitory activity

TrkB induced metastatic potential of cancer by suppression of BMP mediated tumor inhibitory activity

BMP6/TAZ-Hippo signaling modulates angiogenesis and endothelial cell response to VEGF

KCTD11 inhibits growth and metastasis of hepatocellular carcinoma through activating Hippo signaling

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