IC-2 Suppresses Proliferation and Induces Apoptosis of Bladder Cancer Cells via the Wnt/β-Catenin Pathway

Wu, Lingfeng; He, Shunliang; He, Yi; Wang, Xueping; Lu, Linfeng

doi:10.12659/msm.910742

Cited by 11 publications

(11 citation statements)

References 25 publications

(24 reference statements)

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“…Wnt-C59 (C59), an inhibitor of Wnt, decreased the sphere formation ability of CSCs dosedependently in nasopharyngeal carcinoma (NPC) [151]. IC-2, a novel small-molecule Wnt inhibitor, reduced the population of CD44 + cells (liver CSCs) and the sphereforming ability of hepatocellular carcinoma (HCC) cells, as well as in CRC and bladder cancer cells [152]. In addition, IC-2 increased the sensitivity of 5-FU in the DLD-1 cells, a CRC cell line.…”

Section: Cancer Stem Cells -Wnt/β-catenin Signaling Pathway Inhibitorsmentioning

confidence: 99%

Targeting the Wnt/β-catenin signaling pathway in cancer

2020

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The aberrant Wnt/β-catenin signaling pathway facilitates cancer stem cell renewal, cell proliferation and differentiation, thus exerting crucial roles in tumorigenesis and therapy response. Accumulated investigations highlight the therapeutic potential of agents targeting Wnt/β-catenin signaling in cancer. Wnt ligand/ receptor interface, β-catenin destruction complex and TCF/β-catenin transcription complex are key components of the cascade and have been targeted with interventions in preclinical and clinical evaluations. This scoping review aims at outlining the latest progress on the current approaches and perspectives of Wnt/β-catenin signaling pathway targeted therapy in various cancer types. Better understanding of the updates on the inhibitors, antagonists and activators of Wnt/β-catenin pathway rationalizes innovative strategies for personalized cancer treatment. Further investigations are warranted to confirm precise and secure targeted agents and achieve optimal use with clinical benefits in malignant diseases.

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Section: Cancer Stem Cells -Wnt/β-catenin Signaling Pathway Inhibitorsmentioning

confidence: 99%

Targeting the Wnt/β-catenin signaling pathway in cancer

2020

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“…pullicaecorum -supplemented mice. The expression level of the bladder cancer-associated protein (BLCAP), which is an apoptosis-related tumor suppressor identified from bladder cancer [ 31 , 32 ], was significantly higher (29.2-fold; p < 0.05) in NaB-treated HT1376 cells than that in cells without NaB treatment ( Figure 3 A). Moreover, the immunoreactivity of BLCAP was observed in the layer of transitional epithelium of mouse urinary bladder regardless of whether mice had been treated with B .…”

Section: Resultsmentioning

confidence: 99%

“…At the same time, we observed increased BLCAP in urothelial bladder cells, not only in the HT1376 cells but also in the 5637 cells ( Supplementary Materials Figure S4 ). BLCAP exhibits a tumor suppressor function in various tumors, including urothelial cancer of the bladder [ 31 ] and can reduce cell growth by stimulating apoptosis [ 32 ]. The increase in BLCAP by B .…”

Section: Discussionmentioning

confidence: 99%

Supplementation of Probiotic Butyricicoccus pullicaecorum Mediates Anticancer Effect on Bladder Urothelial Cells by Regulating Butyrate-Responsive Molecular Signatures

Wang

Liu

et al. 2021

Diagnostics

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In bladder cancer, urothelial carcinoma is the most common histologic subtype, accounting for more than 90% of cases. Pathogenic effects due to the dysbiosis of gut microbiota are localized not only in the colon, but also in regulating bladder cancer distally. Butyrate, a short-chain fatty acid produced by gut microbial metabolism, is mainly studied in colon diseases. Therefore, the resolution of the anti-cancer effects of butyrate-producing microbes on bladder urothelial cells and knowledge of the butyrate-responsive molecules must have clinical significance. Here, we demonstrate a correlation between urothelial cancer of the bladder and Butyricicoccus pullicaecorum. This butyrate-producing microbe or their metabolite, butyrate, mediated anti-cancer effects on bladder urothelial cells by regulating cell cycle, cell growth, apoptosis, and gene expression. For example, a tumor suppressor against urothelial cancer of the bladder, bladder cancer-associated protein, was induced in butyrate-treated HT1376 cells, a human urinary bladder cancer cell line. In conclusion, urothelial cancer of the bladder is a significant health problem. To improve the health of bladder urothelial cells, supplementation of B. pullicaecorum may be necessary and can further regulate butyrate-responsive molecular signatures.

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“…Activation of Wnt signaling according to specific cellular environmental stimuli can promote or inhibit apoptosis process 58–60 . A number of reports have shown that Wnt signaling pathway can regulate apoptosis 58,61–64 . Liu et al , identified that nigericin induced apoptosis against CRC via inhibiting Wnt‐related and target proteins 65 .…”

Section: Discussionmentioning

confidence: 99%

Ginkgolide C promotes apoptosis and abrogates metastasis of colorectal carcinoma cells by targeting Wnt/β‐catenin signaling pathway

Yang

Lee

et al. 2021

IUBMB Life

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Ginkgolide C (GGC), isolated from Ginkbiloba, has been reported to display various pharmacological actions, although, anti‐cancer effect of GGC has been poorly understood till now. This study aimed to investigate whether GGC can exhibit anti‐neoplastic effects against colon cancer cells and explore underlying mechanism. The Wnt/β‐catenin signaling can regulate cell proliferation, survival, metastasis, and migration. Wnt/β‐catenin signaling pathway plays important role in colorectal cancer (CRC) and acts as a potential therapeutic target. Abnormal activation of this signaling cascades has been reported in colon CRC. We found that GGC down‐regulated Wnt/β‐catenin signaling cascade. GGC inhibited the expression of Wnt3a, β‐catenin, and β‐catenin down‐stream signals (Axin‐1, p‐GSK3β, and β‐TrCP). Also, GGC suppressed the expression of Wnt/β‐catenin pathway target genes including c‐myc, cyclin D1, and survivin. Additionally, GGC induced apoptosis and suppressed cell proliferation, invasion, and migration. GGC down‐regulated the expressions of matrix metalloproteinase (MMP)‐9 and MMP‐2 proteins. Moreover, silencing of β‐catenin by small interfering RNA (siRNA) enhanced the GGC‐induced apoptosis and inhibitory action of GGC on invasion. Overall, our results indicate that GGC can reduce proliferation and promote apoptosis in colon cancer cells through inhibition of the Wnt/β‐catenin signaling pathway. Thus, GGC can serve as a potent therapeutic agent for management of colon cancer as a novel wnt signaling inhibitor.

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IC-2 Suppresses Proliferation and Induces Apoptosis of Bladder Cancer Cells via the Wnt/β-Catenin Pathway

Cited by 11 publications

References 25 publications

Targeting the Wnt/β-catenin signaling pathway in cancer

Targeting the Wnt/β-catenin signaling pathway in cancer

Supplementation of Probiotic Butyricicoccus pullicaecorum Mediates Anticancer Effect on Bladder Urothelial Cells by Regulating Butyrate-Responsive Molecular Signatures

Ginkgolide C promotes apoptosis and abrogates metastasis of colorectal carcinoma cells by targeting Wnt/β‐catenin signaling pathway

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