Study on the effects of c-erbB-2-specific antisense oligonucleotides on c-erbB-2 overexpressing breast cancer cells

2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 10724-10724
Author(s):  
X. Liu ◽  
P. Fan ◽  
Z. Wu
Keyword(s):  
Breast Cancer ◽  
Flow Cytometry ◽  
Cell Proliferation ◽  
Mtt Assay ◽  
Cell Apoptosis ◽  
Antisense Oligonucleotides ◽  
Therapy Group ◽  
The Other ◽  
Antisense Odns ◽  
Breast Cancer Xenografts

10724 Background: Overexpression of c-erbB2 oncoprotein was always correlated with bad prognostic. In this study, we will research on the effects of c-erbB-2-specific antisense oligonucleotides (ODNs) on c-erbB-2 expression, cell proliferation and apoptosis of c-erbB-2 over-expressing breast cancer TM40D cells, and to further study the effects of c-erbB-2-specific oligonucleotides on breast cancer xenografts in Balb/c mice. Methods: Balb/c mouse derived breast cancer cell line TM40D was incubated with liposome-mediated ODNs for 4 h and cultured for another 72 h, then the effects of ODNs on c-erbB-2 expression, cell proliferation and activation of apoptosis were examined by western blot, MTT assay and flow cytometry. Twenty-six mice with breast cancer xenografts were randomized into three groups—9 in control group, 9 in lipsome group and 8 in therapy group, which were injected hypodermically with 0.1 ml serum-free RPMI-1640 culture-medium, lipsome (10 ug/ml) solution, and the mixture of lipsome solution (10 ug/ml) and anti-sense ODN (1 uM) weekly for consecutive 6 weeks, respectively. After the therapy, the incidence of skin ulcer was recorded, the lumps were removed and weighted, and part of them were used for Flow Cytometry. Results: Western Blotting showed treatment of TM40D cells with c-erbB-2-specific antisense ODNs resulted in inhibition of c-erbB-2 expression. The effects of antisense ODNs on c-erbB-2 protein levels correlated with their effects on cell proliferation. MTT Assay showed antisense ODNs inhibited cell growth by about 50%. Flow cytometry analysis revealed that antisense ODNs increased cell apoptosis by38.5%, compared with cultured cells group 9.13% and liposome group 9.29%. The weight of lumps in the therapy group was significantly lower than that of in the other two groups. Flow Cytometry showed that in the therapy group the ratio of G0/G1 cells in cell cycles was 87.18%, which is higher compared with the other two and proliferation index was lower. Conclusions: Antisense ODNs reduced c-erbB-2 expression, inhibited cell proliferation and induced cell apoptosis. Anti-sense ODNs can inhibit the growth of c-erbB2-overexpressing breast cancer xenogarfts in Balb/c mice. No significant financial relationships to disclose.

ILF3-AS1 promotes cell proliferation and inhibits cell apoptosis of breast cancer by binding with miR-4429 to upregulate RAB14

2021 ◽  
pp. 096032712198942
Author(s):  
Xiaoxue Zhang ◽  
Xianxin Xie ◽  
Kuiran Gao ◽  
Xiaoming Wu ◽  
Yanwei Chen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Breast Cancer Cell ◽  
Cell Apoptosis ◽  
Breast Cancer Cells ◽  
Migration And Invasion ◽  
Cancer Cell Proliferation ◽  
Breast Cancer Cell Proliferation ◽  
Cancer Tissues

As one of the leading causes of cancer-related deaths among women, breast cancer accounts for a 30% increase of incidence worldwide since 1970s. Recently, increasing studies have revealed that the long non-coding RNA ILF3-AS1 is involved in the progression of various cancers. Nevertheless, the role of ILF3-AS1 in breast cancer remains largely unknown. In the present study, we found that ILF3-AS1 was highly expressed in breast cancer tissues and cells. ILF3-AS1 silencing inhibited breast cancer cell proliferation, migration and invasion, and promoted cell apoptosis. ILF3-AS1 bound with miR-4429 in breast cancer cells. Moreover, RAB14 was a downstream target of miR-4429, and miR-4429 expression was negatively correlated with RAB14 or ILF3-AS1 expression in breast cancer tissues. The result of rescue experiments demonstrated that overexpression of RAB14 can reverse the inhibitory effect of ILF3-AS1 knockdown on breast cancer cell proliferation, migration and invasion. Overall, ILF3-AS1 promotes the malignant phenotypes of breast cancer cells by interacting with miR-4429 to regulate RAB14, which might offer a new insight into the underlying mechanism of breast cancer.

scholarly journals Rsf-1 Influences the Sensitivity of Non-Small Cell Lung Cancer to Paclitaxel by Regulating NF-κB Pathway and Its Downstream Proteins

2017 ◽  
Vol 44 (6) ◽  
pp. 2322-2336 ◽  
Author(s):  
Xitao Chen ◽  
Xiaodi Sun ◽  
Jingqian Guan ◽  
Junda Gai ◽  
Jilin Xing ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Flow Cytometry ◽  
Cell Proliferation ◽  
Small Cell Lung Cancer ◽  
Cell Apoptosis ◽  
Small Cell ◽  
Small Cell Lung ◽  
Protein Levels ◽  
H460 Cell ◽  
Xenograft Mice

Background/Aims: The therapeutic efficacy of paclitaxel is hampered by chemotherapeutic resistance in non-small cell lung cancer (NSCLC). Rsf-1 enhanced paclitaxel resistance via nuclear factor-κB (NF-κB) in ovarian cancer cells and nasopharyngeal carcinoma. This study assessed the function of Rsf-1 in the modulation of the sensitivity of NSCLC to paclitaxel via the NF-κB pathway. Methods: The mRNA and protein levels of the related genes were quantified by RT-PCR and Western blotting. Rsf-1 silencing was achieved with CRISPR/Cas9 gene editing. Cell cycle, migration and proliferation were tested with flow cytometry, transwell test and CCK8 test. Cell apoptosis was analyzed with flow cytometry and quantification of C-capase3. The parameters of the tumors were measured in H460 cell xenograft mice. Results: Rsf-1 was highly expressed in H460 and H1299 cells. Rsf-1 knockout caused cell arrest at the G1 phase, increased cell apoptosis, and decreased migration and cell proliferation. Rsf-1 knockout increased the inhibition of cell proliferation, the reduction in cell migration and the augment in cell apoptosis in paclitaxel treated H460 and H1299 cells. Rsf-1 knockout further enhanced the paclitaxel-mediated decrease in the volume and weight of the tumors in H460 cell xenograft mice. Helenalin and Rsf-1 knockout decreased the protein levels of p-P65, BcL2, CFLAR, and XIAP; hSNF2H knockout decreased the protein level of NF-κB p-P65 without altering Rsf-1 and p65 protein levels, while Rsf-1 and hSNF2H double knockout decreased the level of NF-κB p-P65, in H1299 and H460 cells. Conclusion: These results demonstrate that Rsf-1 influences the sensitivity of NSCLC to paclitaxel via regulation of the NF-κB pathway and its downstream genes.

Biological Effects of p53 Mutation W248 and H175 on MCF-7 Cells

2013 ◽  
Vol 790 ◽  
pp. 550-554
Author(s):  
Xiang Yu Zhou ◽  
Ya Jun Liu ◽  
Dan Li
Keyword(s):  
Flow Cytometry ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Tumor Cell ◽  
Mtt Assay ◽  
Biological Effects ◽  
Scratch Test ◽  
Control Group ◽  
Tumor Cell Migration ◽  
Mcf 7

Objective: p53, a tumor suppressor gene, is one of the hotspots in the world of the biomedical field. Mutation of p53 gene, which is found in approximately 50% of human cancers, is a key event in carcinogenesis. This project aims to investigate the new characteristics of two p53 mutants, p53-W248 and p53-H175, in MCF-7 cells, so as to provide the experimental basis for understanding the functional alternations of mutant p53. Methods: In this study, MCF-7 cells transfected with p53-H175 or p53-W248 plasmids were used as experimental group and the MCF-7 cells transfected wild type p53 plasmid were used as control group. Then the biological effects at the cellular level were investigated using 3-(4.5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) assay, flow cytometry analysis and cell scratch test. Results: MTT assay showed that p53-W248 might promote cell proliferation in MCF-7 cells. The results of flow cytometry indicated that no significant effect on cell cycle progression and cell apoptosis by p53-H175 or p53-W248 in cells. The cell scratch test showed that p53-H175 could increase the ability of cell migration. Conclusion: p53-H175 could lead to the promotion of tumor cell migration, while p53-W248 may promote tumor cell proliferation. p53-H175 and p53-W248 might have acquired some new characteristics of oncogenes.

Effects of Simvastatin on Breast Carcinoma Cell Proliferation and Apoptosis via Transforming Growth Factor-β1/Smad3 Pathway

2021 ◽  
Vol 11 (9) ◽  
pp. 1673-1682
Author(s):  
Feng Wang ◽  
Gengbao Qu ◽  
Baokai Wang
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Breast Carcinoma ◽  
Protein Expression ◽  
Breast Cancer Cell ◽  
Cell Apoptosis ◽  
Carcinoma Cell ◽  
Proliferation And Apoptosis ◽  
Smad3 Protein ◽  
Mcf 7

Objective: To investigate the function and causative role of simvastatin (Sim) in breast carcinoma cell apoptosis as well as proliferation. Methods: 20 breast carcinoma patients requiring surgery were treated with Sim (20 days, 30 mg), and samples of pre-treatment (pre) and post-treatment (post) were acquired. We detected tissue cell proliferation and apoptosis changes and used functional experiments to detect cell proliferation and apoptosis changes after treating not only estrogen receptor (ER)-positive (MCF-7) but also ER-negative cells (MDA-MB-231) with Sim or TGF-β1. Detection of p-Smad3 and total Smad3 protein expression changes was conducted, and we finally used in vivo experiments to assess the influence of Sim on breast tumor growth and drug safety. Results: Immunohistochemistry and TUNEL staining results showed that after treatment with Sim, breast carcinoma cell proliferation decreased and apoptosis increased. Functional experiments results showed that Sim notedly promoted the MDA-MB-231 and MCF-7 cell apoptosis, inhibiting migration, proliferation and epithelial mesenchymal transition. Moreover, TGF-β1 protein expression was strikingly lower in Sim group than that in DMSO group. When TGF-β1 and Sim were combined to use, the inhibitory ability of Sim on breast cancer cell proliferation markedly increased and the capability of TGF-β1 protein inducing p-Smad3 protein increased. In addition, after Sim treatment in mice, the tumor volume became smaller, the pathological changes weakened, and there was no significant effect on liver function and kidney function. Conclusion: Sim participates in breast cancer cell apoptosis and proliferation via regulating TGF-β1/Smad3 signal pathway.

Rhein Augments Antiproliferative Effects of Atezolizumab Based on Breast Cancer (4T1) Regression

Planta Medica ◽  
2019 ◽  
Vol 85 (14/15) ◽  
pp. 1143-1149 ◽  
Author(s):  
Zhanyun Shen ◽  
Bo Zhu ◽  
Jiao Li ◽  
Luping Qin
Keyword(s):  
Breast Cancer ◽  
T Cells ◽  
Cd8 T Cells ◽  
Tumour Growth ◽  
The Other ◽  
Treatment Groups ◽  
Tnf Α ◽  
4T1 Breast Cancer ◽  
Apoptotic Factors ◽  
Breast Cancer Xenografts

AbstractRhein, an anthraquinone extracted from rhubarb, is used in traditional Chinese medicine for diuresis, diarrhoea, inflammation, and immune regulation. Atezolizumab, a programmed cell death ligand 1 monoclonal antibody, is mainly used to treat bladder cancer and non-small cell lung cancer unresponsive to chemotherapy. We explored the effects of rhein and atezolizumab in combination on breast cancer. Mice with established 4T1 breast cancer xenografts were administered rhein (10 mg/kg) and atezolizumab (10 mg/kg), alone and in combination, and the effects on tumour growth were evaluated. The proportion of CD8+ T cells in the spleen and tumour tissue, the levels of TNF-α, and interleukin-6 in serum as well as the mRNA levels of apoptotic factors (caspase-3, caspase-8, caspase-9, and Bax/Bcl-2) were also evaluated. All of the treatment groups had inhibitory effects on the xenograft tumour growth, with results that were significantly different from those in the control group. In addition, the proportion of CD8+ T cells in the spleen and tumour was significantly increased in the combination therapy group and was significantly different from the other treatment groups. The serum levels of TNF-α and IL-6 were significantly increased in the rhein and combination therapy groups. Finally, the levels of various apoptotic factors in tumour tissues were significantly higher in the combination treatment group than those in the other groups. Administration of rhein, atezolizumab, or their combination all had therapeutic effects on 4T1 breast cancer xenografts in mice, with the combination treatment having stronger effects.

scholarly journals Anticancer Activity of Binary Toxins from Lysinibacillus sphaericus IAB872 against Human Lung Cancer Cell Line A549

2014 ◽  
Vol 9 (1) ◽  
pp. 1934578X1400900
Author(s):  
Wenjuan Luo ◽  
Cuicui Liu ◽  
Ruijuan Zhang ◽  
Jianwei He ◽  
Bei Han
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Tumor Cell ◽  
Cancer Cells ◽  
Mtt Assay ◽  
Cell Apoptosis ◽  
Human Lung ◽  
Immunocytochemical Staining ◽  
Lysinibacillus Sphaericus ◽  
Proliferative Effect

The inhibitory effect of binary toxic (Bin) protein produced by Lysinibacillus sphaericus IAB872 on cell proliferation of human lung, liver, stomach and cervical tumor cell lines was assessed using MTT assay. The effect of Bin protein on A549 cell proliferation, apoptosis, cell cycle, migration and invasion were examined by MTT assay, Western blotting, Immunocytochemical staining, flow cytometry assay and wound-healing assay. Results showed that Bin protein inhibits proliferation of a range of human cancer cells in vitro. The anti-proliferative effect of Bin is associated with cell apoptosis as a result of an increased ratio of cellular Bax/bcl-2, up-regulated CyclinB1and down-regulated Cdc25c expression, and its anti-proliferative action was associated with cell cycle arrest in the G2/M-phase. Bin protein could promote apoptosis and inhibit motility and invasion of A549 cancer cells. The anti-proliferative effect of Bin protein was associated with the induction of apoptotic cell death and cell cycle disruption. These results show that Bin protein has the potential to be developed as a chemotherapeutic agent by induction of human tumor cell apoptosis.

scholarly journals Functional Analysis of CD99 Upregulation in Acute Myeloid Leukemia

Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 5129-5129
Author(s):  
Vijaya Pooja Vaikari ◽  
Jiawen Yang ◽  
Mojtaba Akhtari ◽  
Houda Alachkar
Keyword(s):  
Flow Cytometry ◽  
Cell Proliferation ◽  
Acute Myeloid Leukemia ◽  
Cell Migration ◽  
Murine Model ◽  
Cell Apoptosis ◽  
Myeloid Leukemia ◽  
Cell Aggregation ◽  
And Migration ◽  
Acute Myeloid

Abstract Background: Acute Myeloid Leukemia (AML) is a hematological malignancy with a 5-yr survival rate of 27%. This indicates an urgent need to identify better therapies. We previously analyzed various gene expression data sets of normal hematopoietic vs AML cells and reported that CD99 is upregulated in AML. CD99 loss of function by siRNA or monoclonal antibody decreased proliferation and migration of AML cells (Vaikari et al, ASH abstract, 2016). Recently, we have also shown that AML blasts transduced with CD99 overexpressing lentivirus exhibit a significant increase in cell proliferation (Vaikari et al, ASH abstract, 2017). Here we further expand our preclinical investigation to study the functional role of CD99 in AML. Methods: We performed lenti-viral transduction to overexpress CD99 (CD99 OE) or empty vector (EV) in THP-1, U937, and MOLM-13 AML cell lines. Proliferation assay was performed by seeding 1X105 cells/mL and measuring cell proliferation using trypan blue at 72 hours. Aggregation assay was performed by seeding 1X105CD99 OE (or EV) cells in a 6 well plate and images for cell aggregation were taken 6 hours later. For the differentiation and apoptosis assays, CD99 OE (or EV) (5X105 cells/mL) were starved overnight. Flow cytometry analyses for CD11b and Annexin-V PI were performed 24 hours later. To determine the effect of CD99 overexpression on cell migration, THP-1, U937, and MOLM-13 (1X105 cells) CD99 OE or EV cells were seeded in a transwell chamber for 4 hours and migration towards SDF-1a was analyzed. For the THP-1 and MOLM-13 murine model, 2.5 X106 cells overexpressing CD99 or EV (n=3 for each) were engrafted into NOD-scid /Il2rg-/- (NSG) mice. Bone marrow (BM) and peripheral blood (PB) were collected to determine engraftment by hCD45 staining through flow cytometry. Results: Transducing cells with CD99 resulted in increased cell proliferation as compared with their respective controls in THP-1 (CD99 OE vs EV: 1.78 fold, p<0.0001), U937 (CD99 OE vs EV: 1.56 fold, p<0.0001), and in MOLM-13 cells (CD99 OE vs EV: 1.87 fold, p<0.0001). THP-1, MOLM-13 and U937 cells stably overexpressing CD99 displayed higher cell aggregation capacity compared to EV cells. Cells stably overexpressing CD99 showed an increase in CD11b expression in THP-1 (CD99 OE vs EV: 2.055-fold, p=0.0027), U937 (CD99 OE vs EV: 1.56-fold, p=0.01), and MOLM-13 cells (CD99 OE vs EV: 1.89- fold, p<0.0001). Cell aggregation was also accompanied by an increase in cell apoptosis of CD99 OE cells in THP-1(CD99 OE vs EV: 3.48-fold, p=0.001), U937 (CD99 OE vs EV: 3.68-fold, p=0.11), and MOLM-13 cells (CD99 OE vs EV: 6.56-fold, p=0.0001). Additionally, CD99 overexpression decreased cell migration compared with EV cells in THP-1(CD99 OE vs EV: 67% decrease, p<0.0001), U937 (CD99 OE vs EV: 75% decrease, p<0.0001), and MOLM-13 cells (CD99 OE vs EV: 73% decrease, p=0.0003). Based on these results, we hypothesize that homotypic interaction of CD99 could play a role in its signaling process in AML. In both the THP-1 and MOLM-13 murine model, mice engrafted with CD99 OE cells had smaller spleens compared with EV mice. In the THP-1 murine model, CD99 OE mice had significantly less engraftment compared with the EV mice in the BM (6.69 vs 14 %, p=0.047), and PB (3.61 vs 91.67%, p<0.0001). Similarly, in the MOLM-13 murine model, hCD45 flow analysis revealed that CD99 OE mice have significantly less engraftment compared with the EV mice in the BM (39.83 vs 71.43%, p=0.0022), and PB (19.43 vs 67.13 %, p=0.018). Conclusion: In summary, our results suggests that even though CD99 enhances AML cell proliferation, it also enhances homotypic cell interaction and cell aggregation, which results in increased cell apoptosis as well as a decrease in cell migration and possibly responsible for the decrease leukemia engraftment. Further investigations are ongoing to determine the effect of homotypic interaction of CD99 in AML. Disclosures No relevant conflicts of interest to declare.

scholarly journals In Vitro Cytotoxic Study and Detection of Apoptosis on Breast Cancer Cell lines MDA-MB 231 after Exposed to Azadirachta Indica A. Juss (neem) Extract

2013 ◽  
Vol 2 (2) ◽  
pp. 80 ◽  
Author(s):  
Dessy Arisanty
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Mtt Assay ◽  
Azadirachta Indica ◽  
Cell Apoptosis ◽  
Ethanol Extract ◽  
Tunel Assay ◽  
Neem Extract

AbstrakSuatu senyawa obat dapat menjadi kemoterapi kanker adalah dengan cara menskrining terlebih dahulu tumbuhan obat yang berpotensi sebagai obat antikanker. Salah satunya adalah tanaman obat daun nimba (Azadirachta indica L.Juss) yang terbukti secara significant menyebabkan apoptosis pada beberapa jenis sel line kanker. Dalam penelitian ini, ekstrak ethanol dari A. indica dipelajari untuk melihat efeknya pada pertumbuhan sel kanker payudara manusia jenis MDA-MB-231 dengan menggunakan tes untuk proliferasi yaitu MTT assai dan untuk mengetahui perubahan morphologi dari apoptosis selnya dengan menggunakan TUNEL assay Ekstrak daun nimba (A. indica) dapat menurunkan keberadaan jumlah sel kanker dengan cara menghambat perkembangan daripada sel tersebut dan menginduksi proses apoptosis pada sel kanker tersebut. Hasil pemeriksaan MTT assai didapatkan nilai IC50 nya adalah 55 ug / mL. Kematian MDA-MB231 sel yang disebabkan oleh ekstrak daun nimba (A.indica) ditemukan melalui mekanisme apoptosis yang secara morfologinya menunjukan ciri ciri dari kematian secara apoptosis seperti kondensasi dari nucleus, membrane nukleus yang melebur dan akhirnya terjadinya fragmentasi dari DNA. Analisis struktur dalaman sel juga mengungkapkan karakteristik apoptosis yaitu marginasi dari kromosom yang disertai dengan fragmentasi DNA dan selanjutnya akan terbentuk badan apoptotik pada sel kanker yang diinkubasi dengan ekstrak tersebut. Pada penelitian ini juga dijumpai peningkatan jumlah sel apoptosis dari hari 1 sampai hari 3 inkubasi oleh ekstrak nimba. Ekstrak ethanol A.indica mungkin mengandung senyawa bioaktif(s) yang menyebabkan kanker payudara MDA-MNB 231 mengalami kematian sel secara apoptosis. Penelitian lebih lanjut masih diperlukan untuk mengetahui mekanisme tumbuhan ini membunuh sel kanker MDA-MB 231.Kata kunci: Studi In vitro, Azadirachta indica, apoptosis, TUNEL assayAbstractA screening is conducted on plants that have potential as anticancer is a promising way for discovering novel chemotherapeutic compound. A medicinal plant neem leaf (Azadirachta indica L.Juss) intake has been shown to induce significant levels of apoptosis in various cancer cells. In this present study, ethanol extract of Azadirachta indica was studied for its effects on growth in MDA-MB 231 human breast cancer cells using assays for proliferation (MTT assay) and mechanisme of cell apoptosis using TUNEL assay. Neem leaf extract decreased cell viability, inhibited cell proliferation, and induced cell apoptosis. Result of MTT assay was 55 μg/mL of neem remarkably reduced cell viability of MDA-MB 231 cells. MDA-MB231 cell death elicited by the extract was found to be apoptotic in nature based the indication of nucleus condensation, shrinkage of nucleus membrane and also DNA fragmentation which are a hallmark of apoptosis. In addition, ultrastructural analysis also revealed apoptotic characteristics which are the presence of chromatin margination and apoptotic bodies in the extract-treated cells. There was an increase in the number of apoptotic cells from day 1 to day 3 post incubation with neem extract. Thus, the results from this study strongly suggest that the ethanol extract of A.indica may contain bioactive compound(s) that caused breast carcinoma, MDA-MNB 231 cell death by apoptosis. It’s needed to do advance research to know more deeply the mechanism this plant on breast cancer cell line MDA-MB.Keywords:In vitro study, Azadirachta indica, apoptosis, TUNEL assay

scholarly journals DCTPP1, an Oncogene Regulated by miR-378a-3p, Promotes Proliferation of Breast Cancer via DNA Repair Signaling Pathway

2021 ◽  
Vol 11 ◽  
Author(s):  
Ming Niu ◽  
Ming Shan ◽  
Yang Liu ◽  
Yanni Song ◽  
Ji-guang Han ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Dna Repair ◽  
Survival Rates ◽  
The Other ◽  
Poor Survival ◽  
Induced Apoptosis ◽  
Cell Growth And Proliferation

Breast cancer (BRCA) is one of the most deadly cancers worldwide, with poor survival rates that could be due to its high proliferation. Human all-alpha dCTP pyrophosphatase 1 (DCTPP1) is implicated in numerous diseases, including cancers. However, its role in BRCA is unclear. In this study, we used bioinformatic analyses of the ONCOMINE, UALCAN, and GEPIA databases to determine the expression pattern of DCTPP1 in BRCA. We found that elevated DCTPP1 levels correlate with poor BRCA prognosis. DCTPP1 silencing inhibited BRCA cell proliferation and induced apoptosis in vitro, as well as in vivo. Our data show that this tumorigenic effect depends on DNA repair signaling. Moreover, we found that DCTPP1 is directly modulated by miR-378a-3p, whose downregulation is linked to BRCA progression. Our results showed down-regulation of miR-378a-3p in BRCA. Upregulation of miR-378a-3p, on the other hand, can inhibit BRCA cell growth and proliferation. This study shows that reduced miR-378a-3p level enhances DCTPP1 expression in BRCA, which promotes proliferation by activating DNA repair signaling in BRCA.

Sign in / Sign up

Export Citation Format

Share Document