scholarly journals NDRG2 Expression in Breast Cancer Cells Downregulates PD-L1 Expression and Restores T Cell Proliferation in Tumor-Coculture

Cancers ◽  
2021 ◽  
Vol 13 (23) ◽  
pp. 6112
Author(s):  
Aram Lee ◽  
Soyoung Lim ◽  
Juyeong Oh ◽  
Jihyun Lim ◽  
Young Yang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
T Cell ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Linear Regression Analysis ◽  
T Cell Proliferation ◽  
Breast Cancer Patients ◽  
Ndrg2 Expression ◽  
Malignant Breast

(1) Background: The aim of the present study was to evaluate the effect of NDRG2 expression in regulating PD-L1 or PD-L2 on malignant breast cancer cells. (2) Methods: Overexpression and knockdown of the NDRG2 gene in human and mouse cancer cells were applied and quantitative real-time PCR and Western blot analysis were performed. T cell proliferation and TCGA analysis were conducted to validate negative correlation of the PD-L1 expression with the NDRG2 expression. (3) Results: We found that NDRG2 overexpression inhibits PD-L1 expression in human breast cancer cells through NF-κB signaling. NDRG2 overexpression in 4T1 mouse breast cancer cells followed by PD-L1 downregulation could block the suppressive activity of cancer cells on T cell proliferation and knockdown of NDRG2 expression enhanced the expression of PD-L1, leading to the inhibition of T cell proliferation by tumor cell coculture. Finally, we confirmed from TCGA data that PD-L1 expression in basal and triple-negative breast cancer patients was negatively correlated with the expression of NDRG2. Intriguingly, linear regression analysis using TNBC cell lines showed that the PD-L1 level was negatively associated with the NDRG2 expression level. (4) Conclusions: Our findings demonstrate that NDRG2 expression is instrumental in suppressing PD-L1 expression and restoring PD-L1-inhibited T cell proliferation activity in TNBC cells.

scholarly journals MiR-92b-3p Inhibits Proliferation of HER2-Positive Breast Cancer Cell by Targeting circCDYL

2021 ◽  
Vol 9 ◽  
Author(s):  
Gehao Liang ◽  
Yun Ling ◽  
Qun Lin ◽  
Yu Shi ◽  
Qing Luo ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Biological Function ◽  
Breast Cancer Tissue ◽  
Cancer Tissue ◽  
Breast Cancer Patients ◽  
Her2 Positive ◽  
Over Expression

ObjectivesCircular RNA (circRNA) is a novel class of RNA, which exhibits powerful biological function in regulating cellular fate of various tumors. Previously, we had demonstrated that over-expression of circRNA circCDYL promoted progression of HER2-negative (HER2–) breast cancer via miR-1275-ULK1/ATG7-autophagic axis. However, the role of circCDYL in HER2-positive (HER2+) breast cancer, in particular its role in modulating cell proliferation, one of the most important characteristics of cellular fate, is unclear.Materials and methodsqRT-PCR and in situ hybridization analyses were performed to examine the expression of circCDYL and miR-92b-3p in breast cancer tissues or cell lines. The biological function of circCDYL and miR-92b-3p were assessed by plate colony formation and cell viability assays and orthotopic animal models. In mechanistic study, circRNAs pull-down, RNA immunoprecipitation, dual luciferase report, western blot, immunohistochemical and immunofluorescence staining assays were performed.ResultsCircCDYL was high-expressed in HER2+ breast cancer tissue, similar with that in HER2– breast cancer tissue. Silencing HER2 gene had no effect on expression of circCDYL in HER2+ breast cancer cells. Over-expression of circCDYL promoted proliferation of HER2+ breast cancer cells but not through miR-1275-ULK1/ATG7-autophagic axis. CircRNA pull down and miRNA deep-sequencing demonstrated the binding of miR-92b-3p and circCDYL. Interestingly, circCDYL did not act as miR-92b-3p sponge, but was degraded in miR-92b-3p-dependent silencing manner. Clinically, expression of circCDYL and miR-92b-3p was associated with clinical outcome of HER2+ breast cancer patients.ConclusionMiR-92b-3p-dependent cleavage of circCDYL was an essential mechanism in regulating cell proliferation of HER2+ breast cancer cells. CircCDYL was proved to be a potential therapeutic target for HER2+ breast cancer, and both circCDYL and miR-92b-3p might be potential biomarkers in predicting clinical outcome of HER2+ breast cancer patients.

mir-556-3p Promotes the Progression of Breast Cancer Through Targeting Disabled Gene Homolog 2 Interacting Protein (DAB2IP)

2021 ◽  
Vol 11 (12) ◽  
pp. 2472-2477
Author(s):  
Chunxiong Fan ◽  
Yanping Deng ◽  
Yaqing Liu ◽  
Xiaoying Liu ◽  
Xi Ke ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Cell Activity ◽  
Control Group ◽  
Cancer Tissue ◽  
Breast Cancer Patients ◽  
Cancer Pathogenesis

Our study assessed miR-556-3p’s role in breast cancer cells. A total of 65 cases of breast cancer tissue samples were retrospectively analyzed to detect miR-556-3p level by PCR and analyze survival time and 30 normal breast tissues were included as a control group. Breast cancer cells were cultured followed by analysis of cell proliferation by MTT, cell invasion by transwell assay. miR-556-3p level was significantly upregulated in breast cancer patients compared to control group (P <0.05) and inversely associated with survival rate (P <0.05). In vitro experiments, cell activity and invasion were positively correlated with miR-556-3p level (P <0.05). In MCF-7 cell lines, miR-556-3p overexpression increased cell activity (P <0.05). Meanwhile, after miR-556-3p was overexpressed, the expression of DAB2IP, Erk, p-Erk in breast cancer cells was significantly reduced and increased after miR-556-3p was knocked down. In conclusion, miR-556-3p targets DAB2IP3′-UTR, promotes breast cancer cell proliferation, indicating that miR-556-3p might be involved in breast cancer pathogenesis and may be a new target for the treatment.

CD14+ HLA-DR−/low MDSCs are elevated in the periphery of early-stage breast cancer patients and suppress autologous T cell proliferation

2017 ◽  
Vol 168 (2) ◽  
pp. 401-411 ◽  
Author(s):  
Lisa Speigl ◽  
Helen Burow ◽  
Jithendra Kini Bailur ◽  
Nicole Janssen ◽  
Christina-Barbara Walter ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
T Cell ◽  
Cancer Patients ◽  
Early Stage ◽  
Early Stage Breast Cancer ◽  
T Cell Proliferation ◽  
Breast Cancer Patients ◽  
Hla Dr

scholarly journals Inhibiting of TACC3 Promotes Cell Proliferation, Cell Invasion and the EMT Pathway in Breast Cancer

2021 ◽  
Vol 12 ◽  
Author(s):  
Qin Huo ◽  
Siqi Chen ◽  
Zhenwei Li ◽  
Juan Wang ◽  
Jiaying Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Coiled Coil ◽  
Growth Factor Receptor ◽  
Prognostic Index ◽  
Her2 Status ◽  
Breast Cancer Patients

Accumulating evidences indicate that transforming acidic coiled-coil 3 (TACC3) is a tumor-related gene, was highly expressed in a variety of human cancers, which is involved in cancer development. However, the potential role of TACC3 in breast cancer remains largely unknown. In the present study, we found that TACC3 was highly-expressed in breast cancer tissues, and its level was positively correlated with the clinical features of breast cancer patients. Specifically, TACC3 expression was significantly associated with the estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor 2 (HER2) status, nodal status, the scarff-bloom-richardson (SBR) grade, nottingham prognostic index (NPI), age, subtypes, and triple-negative and basal-like status, suggesting that TACC3 may be a potential diagnostic indicator of breast cancer. Furthermore, functional studies have shown that inhibition of TACC3 can significantly promote the cell proliferation and viability of breast cancer cells. Moreover, TACC3 knockdown suppressed the expression of E-cadherin, but increased the expression of N-cadherin, Snail, ZEB1, and TWIST, which indicate that TACC3 may impact the migration of breast cancer cells in vitro. Taken together, these findings indicate that TACC3 may serve as a prognostic and therapeutic indicator of breast cancer.

scholarly journals Polarity Protein Par3 Sensitizes Breast Cancer to Paclitaxel by Promoting Cell Cycle Arrest.

2021 ◽  
Author(s):  
She Chen ◽  
Yannan Zhao ◽  
Huitong Peng ◽  
Limiao Liang ◽  
Yi Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Breast Cancer Cells ◽  
Brdu Incorporation ◽  
Individual Treatment ◽  
Breast Cancer Patients ◽  
Kaplan Meier

Abstract Purpose Paclitaxel, belongs to tubulin-binding agents (TBAs), showed a great efficacy against breast cancer via stabilizing microtubules. Drug resistance limits its clinical application. Here we aimed to explore a role of Polarity protein Par3 in improving paclitaxel effectiveness.Methods Breast cancer specimens from 45 patients were collected to study the relationship between Par3 expression and paclitaxel efficacy. The Kaplan–Meier method was used for survival analysis. Cell viability was measured in breast cancer cells (SK-BR-3 and T-47D) with Par3 over-expression or knockdown. The flow cytometry assays were performed to measure cell apoptosis and cell cycle. BrdU incorporation assay and Hoechst 33258 staining were performed to measure cell proliferation and cell apoptosis, respectively. Immunofluorescence was used to detect microtubule structures. Results Par3 expression is associated with good response of paclitaxel in breast cancer patients. Consistently, Par3 overexpression significantly sensitizes breast cancer cells to paclitaxel by promoting cell apoptosis and reducing cell proliferation. In Par3 overexpressing cells upon paclitaxel treatment, we observed intensified cell cycle arrests at metaphase. Further exploration showed that Par3 overexpression stabilizes microtubules of breast cancer cells in response to paclitaxel, and resists to microtubules instability induced by nocodazole, a microtubule-depolymerizing agent. Conclusion Par3 facilitates polymeric forms of tubulin and stabilizes microtubule structure, which aggravates paclitaxel-induced delay at the metaphase-anaphase transition, leading to proliferation inhibition and apoptosis of breast cancer cells. Par3 has a potential role in sensitizing breast cancer cells to paclitaxel, which may provide a more precise assessment of individual treatment and novel therapeutic targets.

scholarly journals TNFRSF9 Suppressed the Progression of Breast Cancer via the p38MAPK/PAX6 Signaling Pathway

2022 ◽  
Author(s):  
Xun Zhu ◽  
Xiaorong Liu ◽  
Yehui Zhou ◽  
Chenglin Qin
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Immune Modulation ◽  
Breast Cancer Cells ◽  
Cancer Drug ◽  
The Novel ◽  
Breast Cancer Patients ◽  
Immunotherapy Target ◽  
Cancer Tissues

Abstract Background Worldwide, Breast cancer is the most common cancer in females. Endocrine therapy can effectively treat 85% of breast cancer patients, but 15% of patients could only be treated with chemotherapy and surgery, and the prognosis is much worse. Immunotherapy is the novel treatment for breast cancer that PD-1 and CTLA-4 antibodies have shown evidence of immune modulation in breast cancer drug trials. Methods and Result In this study, we report that TNFRSF9 regulates the cell proliferation, invasion, and apoptosis of breast cancer cells through regulating the phosphorylation of p38, thus further regulate the expression of PAX6. In both breast cancer tissues and cell lines, the levels of TNFRSF9 are significantly decreased, and breast cancer cell development will be promoted with knockdown of TNFRSF9. Moreover, we identify that downregulation of TNFRSF9 can upregulate the phosphorylated p38 (p-p38) and PAX6. We further elucidate that p-p38 is essential for PAX6 expression that p38 phosphorylation inhibitor can reverse the upregulation of PAX6 and suppress cell proliferation, invasion, and promote apoptosis in breast cancer cells. Conclusions In summary, this study proposed a novel TNFRSF9/p38/PAX6 axis that contributes to tumor suppression, which suggests a potential immunotherapy target for breast cancer.

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