Correction: Author Correction: Menin enhances c-Myc-mediated transcription to promote cancer progression

Wu, Gongwei; Yuan, Mengqiu; Shen, Shengqi; Ma, Xiaoyu; Fang, Jingwen; Zhu, Lianbang; Sun, Linchong; Liu, Zhaoji; He, Xiaoping; Huang, De; Li, Tingting; Li, Chenchen; Wu, Jun; Hu, Xin; Li, Zhaoyong; Song, Libing; Qu, Kun; Zhang, Huafeng; Gao, Ping

doi:10.1038/ncomms16195

Cited by 3 publications

(2 citation statements)

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“…The survivin protein functions to inhibit caspase activation, thereby leading to negative regulation of apoptosis or programmed cell death, which has been confirmed by disruption of survivin induction pathways leading to increase in apoptosis and decrease in tumour growth. Enlargement and tumorigenesis of CRC was strengthened through the expression of many genes including c-myc, CyclinD1 and survivin (30). Particularly, the plant products effectively inhibit the β-catenin expression and the tumor formation in CRC cells (31)(32)(33).…”

Section: Discussionmentioning

confidence: 99%

Wnt/β-catenin signaling pathway is involved in induction of apoptosis by oridonin in colon cancer COLO205 cells

Bu¹,

Liu²,

Cui³

et al. 2019

Transl. Cancer Res.

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Background: Oridonin has been demonstrated to have anticancer effect on all kinds of cancer cells and it has shown anti-tumor activity in some tumors partially via the inactivation of Wnt/β-catenin signaling pathway. The study investigated the anticancer effect of oridonin on colon carcinoma cell line COLO205 and explored underlying mechanism.Methods: Cell Counting Kit-8 (CCK-8) assay was performed to assess cell viability. Flow cytometry was performed to analyze the apoptosis. The key target genes and proteins involved in Wnt/β-catenin pathway were detected by quantitative polymerase chain reaction (qPCR) and Western blotting. The xenograft tumor model of colon cancer COLO205 cell was introduced to detect anti-tumor effects in vivo. Transferasemediated dUTP nick end labeling (TUNEL) assay was adopted to test the apoptotic cells in the tumor tissues.Results: Oridonin inhibited the proliferation of colon cancer COLO205 cells in a dose-dependent and time-dependent manner. Oridonin induced apoptosis by increasing the cleavage of caspases in vitro.Furthermore, the expression levels of β-catenin and its downstream targets, including c-myc, cyclinD1 and survivin were significantly reduced. Nevertheless the knockdown of β-catenin by specific small interfering RNA (siRNA) could augment the anti-proliferative and pro-apoptotic effects by oridonin in COLO205 cells.Meanwhile, oridonin also increased protein expression level of glycogen synthase kinase 3β (GSK3β) and decreased the phosphorylation level of GSK3β. In vivo, oridonin treatment significantly suppressed tumor growth of COLO205 cell xenografts, and which was accompanied by the restrain of Wnt/β-catenin pathway.Conclusions: Our present study demonstrated that the growth inhibition and apoptosis induction in colon cancer COLO205 cells by oridonin could be partially mediated through discontinuing Wnt/β-catenin signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Wnt/β-catenin signaling pathway is involved in induction of apoptosis by oridonin in colon cancer COLO205 cells

Bu¹,

Liu²,

Cui³

et al. 2019

Transl. Cancer Res.

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“…64 However, it interacts with myelocytomatosis oncogene (MYC) and enhances the transcription of MYC target genes independent from H3K4me3 inhibitory activity. 65 Menin inhibits SHH 66 and HOX signaling via PRMT5. It interacts with CHES1 in S-phase checkpoint pathway related to DNA damage response.…”

Section: Multiple Endocrine Neoplasia Type 1 (Men1)mentioning

confidence: 99%

Pathological Features of Tumors of the Nervous System in Hereditary Cancer Predisposition Syndromes: A Review

et al. 2021

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Hereditary cancer predisposition syndromes (HCS) become more recognizable as the knowledge about them expands, and genetic testing becomes more affordable. In this review, we discussed the known HCS that predispose to central and peripheral nervous system tumors. Different genetic phenomena were highlighted, and the important cellular biological alterations were summarized. Genetic mosaicism and germline mutations are features of HCS, and recently, they were described in normal population and as modifiers for the genetic landscape of sporadic tumors. Description of the tumors arising in these conditions was augmented by representative cases explaining the main pathological findings. Clinical spectrum of the syndromes and diagnostic criteria were tabled to outline their role in defining these disorders. Interestingly, precision medicine has found its way to help these groups of patients by offering targeted preventive measures. Understanding the signaling pathway alteration of mammalian target of rapamycin (mTOR) in tuberous sclerosis helped introducing mTOR inhibitors as a prophylactic treatment in these patients. More research to define the germline genetic alterations and resulting cellular signaling perturbations is needed for effective risk-reducing interventions beyond prophylactic surgeries.

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Raddeanin A inhibits growth and induces apoptosis in human colorectal cancer through downregulating the Wnt/β-catenin and NF-κB signaling pathway

et al. 2018

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Correction: Author Correction: Menin enhances c-Myc-mediated transcription to promote cancer progression

Cited by 3 publications

References 0 publications

Wnt/β-catenin signaling pathway is involved in induction of apoptosis by oridonin in colon cancer COLO205 cells

Wnt/β-catenin signaling pathway is involved in induction of apoptosis by oridonin in colon cancer COLO205 cells

Pathological Features of Tumors of the Nervous System in Hereditary Cancer Predisposition Syndromes: A Review

Raddeanin A inhibits growth and induces apoptosis in human colorectal cancer through downregulating the Wnt/β-catenin and NF-κB signaling pathway

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