Inhibition of β‐catenin/Tcf signaling by flavonoids

Park, Sung Yong; Choi, Jae Min

doi:10.1002/jcb.22654

Cited by 59 publications

(49 citation statements)

References 32 publications

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“…Many factors have been identified as cotranscription factors in this signaling pathway. They are known to bind TCF-4 or b-catenin and function as transcription coactivators or inhibitors (27)(28)(29). In our previous study, we found that SPINDLIN1 interacts with TCF-4 and activates its activity (19), suggesting that SPINDLIN1 might promote cancer cell proliferation via this signaling pathway.…”

Section: Discussionmentioning

confidence: 90%

SPINDLIN1 Promotes Cancer Cell Proliferation through Activation of WNT/TCF-4 Signaling

Wang¹,

Zeng²,

Chen³

et al. 2012

Molecular Cancer Research

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SPINDLIN1, a new member of the SPIN/SSTY gene family, was first identified as a gene highly expressed in ovarian cancer cells. We have previously shown that it is involved in the process of spindle organization and chromosomal stability and plays a role in the development of cancer. Nevertheless, the mechanisms underlying its oncogenic role are still largely unknown. Here, we first showed that expression of SPINDLIN1 is upregulated in clinical tumors. Ectopic expression of SPINDLIN1 promoted cancer cell proliferation and activated WNT/T-cell factor (TCF)-4 signaling. The Ser84 and Ser99 amino acids within SPINDLIN1 were further identified as the key functional sites in WNT/TCF-4 signaling activation. Mutation of these two sites of SPINDLIN1 abolished its effects on promoting WNT/TCF-4 signaling and cancer cell proliferation. We further found that Aurora-A could interact with and phosphorylate SPINDLIN1 at its key functional sites, Ser84 and Ser99, suggesting that phosphorylation of SPINDLIN1 is involved in its oncogenic function. Collectively, these results suggest that SPINDLIN1, which may be a novel substrate of the Aurora-A kinase, promotes cancer cell growth through WNT/ TCF-4 signaling activation. Mol Cancer Res; 10(3); 326-35. Ó2012 AACR.

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Section: Discussionmentioning

confidence: 90%

SPINDLIN1 Promotes Cancer Cell Proliferation through Activation of WNT/TCF-4 Signaling

Wang¹,

Zeng²,

Chen³

et al. 2012

Molecular Cancer Research

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“…As consequence Genistein inhibits prostate cancer (Li et al, 2008). Genistein also suppressed β-catenin/Tcf trancriptional activity in SW480 cells (colorectal carcinoma cells) in a dose-dependent manner (Park and Choi, 2010). Genistein affect the upstream components of the β-catenin/Tcf pathway by suppression of GSK-3β and Akt phosphorylation (Park and Choi, 2010).…”

Section: Targeting Wnt/β-catenin With Flavonoidsmentioning

confidence: 97%

Flavonoids: Potential Wnt/beta-catenin signaling modulators in cancer

et al. 2011

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Flavonoids are polyphenolic compounds found throughout the plant kingdom. They occur in every organ but are usually concentrated in leaves and flowers. During the last two decades, in vitro and in vivo studies demonstrated that flavonoids have inhibitory effects on human diseases through targeting of multiple cellular signaling components. Wnt/β-catenin signaling regulates proliferation, differentiation and fate specification in developmental stages and controls tissue homeostasis in adult life. For these reasons, this pathway has received great attention in the last years as potential pathway involved in distinct Human pathologies. In this review we discuss the emerging potential mechanisms for flavonoids on Wnt/β-catenin signaling in cancer and possible investigation strategies to understand flavonoids mode of action on this signaling pathway.

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“…Kaempferol suppressed β-catenin/TCF transcriptional activity in SW480 colon cancer cells, which has inactivating mutation of the APC gene and shows a constitutively active transcriptional activity of β-catenin/TCF. This can further suppress c-Myc and cyclin D1 (Park & Choi, 2010). Naringin also has shown to target β-catenin in breast cancer cells (Li et al, 2013).…”

Section: Fig 4 -Effect Of Methanol Extract Of Amla Seed (As) or Pulpmentioning

confidence: 97%

Indian gooseberry (Emblica officinalis Gaertn.) suppresses cell proliferation and induces apoptosis in human colon cancer stem cells independent of p53 status via suppression of c-Myc and cyclin D1

Vadde

Radhakrishnan

Kurundu

et al. 2016

Journal of Functional Foods

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Available online A B S T R A C TIndian gooseberry, also known as amla, a widely consumed fruit in South Asia, was evaluated for its anti-proliferative and pro-apoptotic mechanisms on human colon cancer stem cells (HCCSC). Amla extracts suppressed proliferation and induced apoptosis independent of p53, a tumour suppressor gene, in HCCSCs. Further, amla extracts suppressed cell proliferation by targeting the Wnt/β-catenin signalling pathway as seen by decreased nuclear translocation of β-catenin. Additionally, this led to suppressed expression of c-Myc and cyclin D1, key proteins involved in cell proliferation. Inhibition of stem-ness of HCCSCs by amla may be due to its effect on the Wnt/β-catenin signalling. These results indicate that amla suppresses HCCSC proliferation and induces apoptosis independent of p53 status via potentially targeting Wnt/β-catenin signalling pathway. Amla is therefore a promising functional food for preventing colon cancer and might be a novel resource for the food industry.

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Inhibition of β‐catenin/Tcf signaling by flavonoids

Cited by 59 publications

References 32 publications

SPINDLIN1 Promotes Cancer Cell Proliferation through Activation of WNT/TCF-4 Signaling

SPINDLIN1 Promotes Cancer Cell Proliferation through Activation of WNT/TCF-4 Signaling

Flavonoids: Potential Wnt/beta-catenin signaling modulators in cancer

Indian gooseberry (Emblica officinalis Gaertn.) suppresses cell proliferation and induces apoptosis in human colon cancer stem cells independent of p53 status via suppression of c-Myc and cyclin D1

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