scholarly journals Chemotherapy-induced S100A10 recruits KDM6A to facilitate OCT4-mediated breast cancer stemness

2020 ◽  
Vol 130 (9) ◽  
pp. 4607-4623 ◽  
Author(s):  
Haiquan Lu ◽  
Yangyiran Xie ◽  
Linh Tran ◽  
Jie Lan ◽  
Yongkang Yang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Stemness

CDK12 Promotes Breast Cancer Progression and Maintains Stemness by Activating c-myc/β -catenin Signaling

2020 ◽  
Vol 20 (2) ◽  
pp. 156-165 ◽  
Author(s):  
Fang Peng ◽  
Chuansheng Yang ◽  
Yanan Kong ◽  
Xiaojia Huang ◽  
Yanyu Chen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Lung Metastasis ◽  
Xenograft Model ◽  
Breast Cancer Cell Lines ◽  
Cell Renewal ◽  
Cancer Stemness ◽  
Mesenchymal Transition ◽  
Potential Biomarker

Background: CDK12 is a promising therapeutic target in breast cancer with an effective ability of maintaining cancer cell stemness. Objective: We aim to investigate the mechanism of CDK12 in maintaining breast cancer stemness. Methods: CDK12 expression level was accessed by using RT-qPCR and IHC. CDK12-altered breast cancer cell lines MDA-MB-231-shCDK12 and SkBr-3-CDK12 were then established. CCK8, colony formation assays, and xenograft model were used to value the effect of CDK12 on tumorigenicity. Transwell assay, mammosphere formation, FACS, and lung metastasis model in vivo were determined. Western blot further characterized the mechanism of CDK12 in breast cancer stemness through the c-myc/β-catenin pathway. Results: Our results showed a higher level of CDK12 exhibited in breast cancer samples. Tumor formation, cancer cell mobility, spheroid forming, and the epithelial-mesenchymal transition will be enhanced in the CDK12high group. In addition, CDK12 was associated with lung metastasis and maintained breast cancer cell stemness. CDK12high cancer cells presented higher tumorigenicity and a population of CD44+ subset compared with CDK12low cells. Our study demonstrated c-myc positively expressed with CDK12. The c-myc/β-catenin signaling was activated by CDK12, which is a potential mechanism to initiate breast cancer stem cell renewal and may serve as a potential biomarker of breast cancer prognosis. Conclusion: CDK12 overexpression promotes breast cancer tumorigenesis and maintains the stemness of breast cancer by activating c-myc/β-catenin signaling. Inhibiting CDK12 expression may become a potential therapy for breast cancer.

Dopamine D1 receptor agonists inhibit lung metastasis of breast cancer reducing cancer stemness

2019 ◽  
Vol 859 ◽  
pp. 172499 ◽  
Author(s):  
Liang Yang ◽  
Ye Yao ◽  
Ling Yong ◽  
Yaoyao Feng ◽  
Hong Su ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Lung Metastasis ◽  
Dopamine D1 Receptor ◽  
D1 Receptor ◽  
Cancer Stemness ◽  
Receptor Agonists

scholarly journals Chemotherapy Induces Breast Cancer Stemness in Association with Dysregulated Monocytosis

2018 ◽  
Vol 24 (10) ◽  
pp. 2370-2382 ◽  
Author(s):  
Liang Liu ◽  
Lin Yang ◽  
Wei Yan ◽  
Jing Zhai ◽  
Donald P. Pizzo ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Stemness

scholarly journals How BMP-2 induces EMT and breast cancer stemness through Rb and CD44?

2018 ◽  
Vol 9 (2) ◽  
Author(s):  
Guanglin Zhang ◽  
Peide Huang ◽  
Anan Chen ◽  
Weiyi He ◽  
Zhen Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Stemness

scholarly journals LncRNA SNHG7 Mediates the Chemoresistance and Stemness of Breast Cancer by Sponging miR-34a

2020 ◽  
Vol 10 ◽  
Author(s):  
Zhi-hua Li ◽  
Ni-si Yu ◽  
Qing Deng ◽  
Yulu Zhang ◽  
Yang-yang Hu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Poor Clinical Outcome ◽  
Cancer Stemness ◽  
Drug Induced ◽  
Sox2 Expression ◽  
Repressive Effect ◽  
Induced Apoptosis ◽  
Cancer Tissues ◽  
Sphere Formation ◽  
Chemoresistant Cell

Chemoresistance is considered to be a major cause of the recurrence and metastasis of breast cancer (BC). LncRNA SNHG7 has been reported to be upregulated in breast cancer and to promote tumor progression and metastasis. Nevertheless, the function and potential regulatory mechanism of SNHG7 in BC drug resistance are still largely unclear. This study indicated that SNHG7 was highly expressed in chemoresistant BC tissues and cells. Upregulated SNHG7 might predict a low pCR rate and poor clinical outcome in BC patients. Knockdown of SNHG7 enhanced drug sensitivity and drug-induced apoptosis in chemoresistant BC cells. In terms of the mechanism, miR-34a was found to be a target of SNHG7 and its expression in breast cancer tissues and chemoresistant cell lines was negatively correlated with SNHG7 expression. Importantly, sh-SNHG7 upregulated miR-34a expression, reduced the percentages of CD44+/CD24−cells, and inhibited sphere-formation and stem cell factor (Oct4, Nanog, SOX2) expression. Functional loss experiments showed that the repressive effect of SNHG7 knockdown on BC cell stemness was partially reversed by transfection with miR-34a inhibitors. In summary, this study indicated that SNHG7 contributed to the chemoresistance of BC and mediated chemoresistance and cancer stemness by sponging miR-34a.

scholarly journals Chronic circadian disruption modulates breast cancer stemness and immune microenvironment to drive metastasis in mice

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Eva Hadadi ◽  
William Taylor ◽  
Xiao-Mei Li ◽  
Yetki Aslan ◽  
Marthe Villote ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Circadian Disruption ◽  
Immune Microenvironment ◽  
Cancer Stemness

scholarly journals The mechanism of how CD95/Fas activates the Type I IFN/STAT1 axis, driving cancer stemness in breast cancer

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Abdul S. Qadir ◽  
Austin M. Stults ◽  
Andrea E. Murmann ◽  
Marcus E. Peter
Keyword(s):  
Breast Cancer ◽  
Type I ◽  
Type I Ifn ◽  
Cancer Stemness
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