Sinomenine hydrochloride suppresses the stemness of breast cancer stem cells by inhibiting Wnt signaling pathway through down-regulation of WNT10B

Li, Xiaomei; Chen, Wei; Huang, Lijie; Zhu, Mengmei; Zhang, Hongxia; Si, Yanna; Li, Hengyu; Luo, Qin; Yu, Bing

doi:10.1016/j.phrs.2022.106222

Cited by 13 publications

(11 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In contrast, WNT1 expression did not predict survival (Wend et al, 2013). WNT10B overexpression in MDA-MB-231 breast cancer stem cells increased tumor size in vivo, and shWNT10B decreased the number of mammospheres and colony-forming units compared to controls, further confirming a role for WNT10B in cancer stem cells (Li X. et al, 2022).…”

Section: Wnt10b and Cancermentioning

confidence: 89%

“…Li et al (2022) interrogated the effects of sinomenine hydrochloride (SH), which is extracted from a Chinese medicinal plant Sinomenium acutum , on breast cancer stem cells (BCSC) ( Li X. et al, 2022 ). SH is known to have anti-inflammatory properties.…”

Section: Wnt10b and Cancermentioning

confidence: 99%

“…The loss of tumor growth coincided with the loss of WNT10B , β-catenin, and canonical WNT target genes ( MYC , JUN , CD44 , and MET ) in BCSCs. Therefore, SH inhibits TNBC in vivo by disrupting WNT10B signaling in BCSCs ( Li X. et al, 2022 ).…”

Section: Wnt10b and Cancermentioning

confidence: 99%

See 2 more Smart Citations

The role of WNT10B in physiology and disease: A 10-year update

Perkins

Singh

Abell

et al. 2023

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

WNT10B, a member of the WNT family of secreted glycoproteins, activates the WNT/β-catenin signaling cascade to control proliferation, stemness, pluripotency, and cell fate decisions. WNT10B plays roles in many tissues, including bone, adipocytes, skin, hair, muscle, placenta, and the immune system. Aberrant WNT10B signaling leads to several diseases, such as osteoporosis, obesity, split-hand/foot malformation (SHFM), fibrosis, dental anomalies, and cancer. We reviewed WNT10B a decade ago, and here we provide a comprehensive update to the field. Novel research on WNT10B has expanded to many more tissues and diseases. WNT10B polymorphisms and mutations correlate with many phenotypes, including bone mineral density, obesity, pig litter size, dog elbow dysplasia, and cow body size. In addition, the field has focused on the regulation of WNT10B using upstream mediators, such as microRNAs (miRNAs) and long non-coding RNAs (lncRNAs). We also discussed the therapeutic implications of WNT10B regulation. In summary, research conducted during 2012–2022 revealed several new, diverse functions in the role of WNT10B in physiology and disease.

show abstract

Section: Wnt10b and Cancermentioning

confidence: 89%

Section: Wnt10b and Cancermentioning

confidence: 99%

See 1 more Smart Citation

The role of WNT10B in physiology and disease: A 10-year update

Perkins

Singh

Abell

et al. 2023

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

show abstract

“…Western blots were performed as described previously ( Li et al, 2022 ). In brief, the total protein was prepared with RIPA buffer (89,901, ThermoFisher), quantified by BCA kit (23,225, ThermoFisher), separated by SDS-PAGE electrophoresis, and was transferred to PVDF membranes.…”

Section: Methodsmentioning

confidence: 99%

Yi-Shen-Hua-Shi Granule Alleviates Adriamycin-Induced Glomerular Fibrosis by Suppressing the BMP2/Smad Signaling Pathway

Tan

Si²,

Yu³

et al. 2022

Front. Pharmacol.

Self Cite

View full text Add to dashboard Cite

Focal segmental glomerulosclerosis (FSGS) is a common clinical condition with manifestations of nephrotic syndrome and fibrosis of the glomeruli and interstitium. Yi-Shen-Hua-Shi (YSHS) granule has been shown to have a good effect in alleviating nephrotic syndrome (NS) in clinical and in animal models of FSGS, but whether it can alleviate renal fibrosis in FSGS and its mechanism and targets are not clear. In this study, we explored the anti-fibrotic effect and the targets of the YSHS granule in an adriamycin (ADR)-induced FSGS model and found that the YSHS granule significantly improved the renal function of ADR-induced FSGS model mice and also significantly reduced the deposition of collagen fibers and the expression of mesenchymal cell markers FN, vimentin, and α-SMA in the glomeruli of ADR-induced FSGS mice, suggesting that the YSHS granule inhibited the fibrosis of sclerotic glomeruli. Subsequently, a network pharmacology-based approach was used to identify the potential targets of the YSHS granule for the alleviation of glomerulosclerosis in FSGS, and the results showed that the YSHS granule down-regulated the expressions of BMP2, GSTA1, GATS3, BST1, and S100A9 and up-regulated the expressions of TTR and GATM in ADR-induced FSGS model mice. We also proved that the YSHS granule inhibited the fibrosis in the glomeruli of ADR-induced FSGS model mice through the suppression of the BMP2/Smad signaling pathway.

show abstract

“…Western blotting assays were performed as previously described [ 23 ]. A dot blot assay was performed as follows: the sample DNA was diluted to final DNA concentrations of 1000 ng/µL, 500 ng/µL and 200 ng/µL.…”

Section: Methodsmentioning

confidence: 99%

Induced hepatic stem cells maintain self-renewal through the high expression of Myc coregulated by TET1 and CTCF

Wang

Ding

et al. 2022

Cell Biosci

Self Cite

View full text Add to dashboard Cite

Background Induced hepatic stem cells (iHepSCs) with the capacities of self-renewal and bidifferentiation into hepatocytes and cholangiocytes were generated from mouse embryonic fibroblasts (MEFs) by lineage reprogramming in our previous research. However, the mechanism of iHepSC self-renewal has not been elucidated. Active demethylation regulated by Tet1 plays an important role in the self-renewal of stem cells, including pluripotent stem cells and adult stem cells. Here, we investigated the role and mechanism of Tet1-regulated demethylation in the self-renewal of iHepSCs. Methods The methylation levels and the expression of Tet1 in iHepSCs and MEFs were analyzed by immunofluorescent staining, quantitative reverse transcription PCR and western blotting. Then, the effects of Tet1 knockdown on the proliferation and self-renewal of iHepSCs were analyzed by CCK8, colony formation, and sphere formation assays. The mechanism by which Tet1 regulates the self-renewal of iHepSCs was investigated by chromatin immunoprecipitation, bisulfite sequence PCR, and methylation-sensitive restriction endonuclease-PCR. Results The high level of 5hmC and the low level of 5mC in iHepSCs were accompanied by high expression of Tet1. After Tet1 expression was knocked down by shRNA in iHepSCs, the proliferation and self-renewal capacities were inhibited, and the expression of Myc was also decreased. The higher expression level of Myc in iHepSCs maintained its self-renewal and was regulated by Tet1, which directly binds to CBS-1 and site A regions of the Myc promoter and demethylates the CpG cytosine. In addition, CTCF also binds to the CBS-1 and site A regions of the Myc promoter and regulates Myc expression along with TET1. Conclusion The self-renewal of iHepSCs was maintained by the higher expression of Myc, which was coregulated by TET1 and CTCF. This study may provide new insights into the self-renewal of stem cells, which can promote the research and application of ‘reprogrammed’ stem cells.

show abstract

Sinomenine hydrochloride suppresses the stemness of breast cancer stem cells by inhibiting Wnt signaling pathway through down-regulation of WNT10B

Cited by 13 publications

References 49 publications

The role of WNT10B in physiology and disease: A 10-year update

The role of WNT10B in physiology and disease: A 10-year update

Yi-Shen-Hua-Shi Granule Alleviates Adriamycin-Induced Glomerular Fibrosis by Suppressing the BMP2/Smad Signaling Pathway

Induced hepatic stem cells maintain self-renewal through the high expression of Myc coregulated by TET1 and CTCF

Contact Info

Product

Resources

About