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 Drug-induced Apoptosis and p53, BCL-2 and BAX Expression in Breast Cancer Tissues In Vivo and in Fibroblast Cells In Vitro

1999 ◽  
Vol 29 (7) ◽  
pp. 323-331 ◽  
Author(s):  
K. Suzuki ◽  
T. Kazui ◽  
M. Yoshida ◽  
T. Uno ◽  
T. Kobayashi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Fibroblast Cells ◽  
Drug Induced ◽  
Induced Apoptosis ◽  
Cancer Tissues

Induction of the death-promoting genebax-? sensitizes cultured breast-cancer cells to drug-induced apoptosis

1996 ◽  
Vol 67 (1) ◽  
pp. 138-141 ◽  
Author(s):  
Christian Wagener ◽  
Ralf C. Bargou ◽  
Peter T. Daniel ◽  
Kurt Bommert ◽  
Markus Y. Mapara ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Drug Induced ◽  
Induced Apoptosis

scholarly journals Overexpression of caspase-3 restores sensitivity for drug-induced apoptosis in breast cancer cell lines with acquired drug resistance

Oncogene ◽  
2001 ◽  
Vol 20 (22) ◽  
pp. 2749-2760 ◽  
Author(s):  
Katrin Friedrich ◽  
Thomas Wieder ◽  
Clarissa Von Haefen ◽  
Silke Radetzki ◽  
Reiner Jänicke ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Drug Resistance ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Caspase 3 ◽  
Breast Cancer Cell Lines ◽  
Drug Induced ◽  
Acquired Drug Resistance ◽  
Induced Apoptosis

scholarly journals miR-3065-3p promotes stemness and metastasis by targeting CRLF1 in colorectal cancer

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Yifan Li ◽  
Jing Xun ◽  
Botao Wang ◽  
Yuan Ma ◽  
Lanqiu Zhang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Loss Of Function ◽  
Cancer Stemness ◽  
Sox2 Expression ◽  
Downstream Target ◽  
Cancer Tissues

Abstract Background Colorectal cancer is one of the most common malignancy in the world. It has been reported that cancer stem cells (CSCs) serve as the primary drivers of tumorigenesis and tumor progression. There is an urgent need to explore novel molecules that regulate CSCs or their signatures. Increasing evidence has shown that miRNAs are involved in tumorigenesis and progression. Here, we aim to explore the regulatory effect and mechanism of miR-3065-3p on the stemness of colorectal cancer. Methods The expression of miR-3065-3p in colorectal cancer and the association of miR-3065-3p expression with prognosis of patients with colorectal cancer were analyzed using TCGA dataset or clinical cases. Gain or loss of function in different models, including colorectal cancer cell lines and orthotopic xenograft or liver metastatic mouse model, were used to investigate the effects of miR-3065-3p on colorectal cancer stemness and metastasis in vitro and in vivo. Cancer stemness was analyzed by detecting the ability of migration and invasion, NANOG, OCT4, and SOX2 expression, ALDH activity and sphere formation. In addition, the interaction of miR-3065-3p and cytokine receptor-like factor 1 (CRLF1) was analyzed theoretically and identified by the luciferase reporter assay. Moreover, the correlation between CRLF1 expression and miR-3065-3p was analyzed in colorectal cancer tissues. Finally, the effect of CRLF1 on the stemness and metastasis of colorectal cancer in vitro and in vivo was assessed. Results In this report, we found that miR-3065-3p was overexpressed in colorectal cancer and that its high expression was associated with poor prognosis of patients with colorectal cancer. miR-3065-3p promotes the stemness and metastasis of colorectal cancer. Furthermore, CRLF1 was the downstream target of miR-3065-3p and inhibited the stemness of colorectal cancer. In addition, CRLF1 expression was negatively correlated with miR-3065-3p in colorectal cancer tissues. And, CRLF1 mediated the effects of miR-3065-3p on promoting stemness of colorectal cancer cells. Conclusion Our data suggest that miR-3065-3p promoted the stemness and metastasis of colorectal cancer by targeting CRLF1. miR-3065-3p might serve as a promising prognostic marker as well as a therapeutic target for colorectal cancer.

The roles of microRNA-328-3p on proliferation and radiotherapy in breast cancer

2021 ◽  
Author(s):  
Ying Shi ◽  
Pengli Jiang ◽  
Jinqiu Li ◽  
Shengnan Xu ◽  
Bin Liu
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Breast Carcinogenesis ◽  
Aberrant Expression ◽  
Induced Apoptosis ◽  
Cancer Tissues ◽  
The Impact

Abstract Objectives MicroRNAs regulates varieties of molecular pathways and involve in breast carcinogenesis. Here both breast cancer cell lines and human breast cancer tissues were used to investigate the roles of miR-328-3p in breast cancer. Methods The impact of miR-328-3p on proliferation of MDA-MB-231 and T47D cells was determined by MTT assay. transwell migration and matrigel invasion assays were performed to evaluate effects of miR-328-3p on migration and invasion of breast cancer cells. Caspase 3/7 activities were measured to examine the impact of miR-328-3p on radiotherapy-induced apoptosis in breast cancer cells. The possible binding site of miR-328-3p was verified by dual-luciferase reporter assay. Quantitative real-time polymerase chain reaction was performed to detect miR-328-3p expression level in breast cancer tissues. Western blot and immunohistochemical studies were used to examine protein expression in breast cancer cells and breast cancer tissue, respectively. Results miR-328-3p involved growth, migration and invasion in breast cancer cells and was associated with radiotherapy sensitivity. MiR-328-3p enhanced radiation-induced apoptosis in breast cancer cells by regulating BAX and Bcl-2 expression. Meanwhile, aberrant expression of miR-328-3p was associated with altered expression of PTEN and p-AKT in breast cancer cells. Further study showed miR-328-3p bound to 3’-UTR of PTEN. In addition, breast cancer tissues showed higher level of miR-328-3p than normal breast tissue and higher level of miR-328-3p was seen in lower stage in breast cancer. Conclusions miR-328-3p displayed essential functions in breast carcinogenesis and might be used to predict radiotherapy response and prognosis in breast cancer.

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