Upregulation of Circulating MiR-21 Expression as a Potential Biomarker for Therapeutic Monitoring and Clinical Outcome in Breast Cancer

Purpose: Estrogen-responsive finger protein (Efp) is amember ofRINGfinger-B box-Coiled Coilfamily and is also a downstream target of estrogen receptor a. Previously, Efp was shown tomediate estrogen-induced cell growth, which suggests possible involvement in the developmentof human breast carcinomas. In this study, we examined expression of Efp in breast carcinomatissues and correlated these findings with various clinicopathologic variables.Experimental Design: Thirty frozen specimens of breast carcinomas were used for immunohistochemistryand laser capture microdissection/real-time PCR of Efp. Immunohistochemistryfor Efp was also done in 151breast carcinoma specimens fixed with formalin and embedded inparaffinwax.Results: Efp immunoreactivity was detected in breast carcinoma cells and was significantlyassociated with the mRNA level (n = 30). Efp immunoreactivity was positively associated withlymph node status or estrogen receptor a status and negatively correlated with histologic gradeor 14-3-3j immunoreactivity (n = 151). Moreover, Efp immunoreactivity was significantly correlatedwith poor prognosis of breast cancer patients, and multivariate analyses of disease-freesurvival and overall survival for151breast cancer patients showed that Efp immunoreactivity wasthe independentmarker.Conclusions: Our data suggest that Efp immunoreactivity is a significant prognostic factor inbreast cancer patients. These findings may account for an oncogenic role of Efp in the tumorprogression of breast carcinoma.

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Decision letter for "Low Z‐4OHtam concentrations are associated with adverse clinical outcome among early stage premenopausal breast cancer patients treated with adjuvant tamoxifen"

10.1002/1878-0261.12865/v1/decision1 ◽

2020 ◽

Keyword(s):

Breast Cancer ◽

Clinical Outcome ◽

Cancer Patients ◽

Early Stage ◽

Adjuvant Tamoxifen ◽

Breast Cancer Patients ◽

Adverse Clinical Outcome ◽

Premenopausal Breast Cancer

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A Study to Evaluate the Safety and Clinical Outcome of Using FR-Mask in Breast Cancer Patients With Radiation-irritated Skin After Radiotherapy

Case Medical Research ◽

10.31525/ct1-nct04190381 ◽

2019 ◽

Author(s):

Keyword(s):

Breast Cancer ◽

Clinical Outcome ◽

Cancer Patients ◽

Breast Cancer Patients

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Faculty Opinions recommendation of p53-mediated senescence impairs the apoptotic response to chemotherapy and clinical outcome in breast cancer.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.717956676.793464863 ◽

2012 ◽

Author(s):

Ygal Haupt ◽

Sue Haupt

Keyword(s):

Breast Cancer ◽

Clinical Outcome ◽

Apoptotic Response ◽

Response To Chemotherapy

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Faculty Opinions recommendation of p53-mediated senescence impairs the apoptotic response to chemotherapy and clinical outcome in breast cancer.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.717956676.793461273 ◽

2012 ◽

Author(s):

Christoph Borner

Keyword(s):

Breast Cancer ◽

Clinical Outcome ◽

Apoptotic Response ◽

Response To Chemotherapy

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

Current Cancer Drug Targets ◽

10.2174/1568009619666191118113220 ◽

2020 ◽

Vol 20 (2) ◽

pp. 156-165 ◽

Cited By ~ 3

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.

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