RNAi-mediated knockdown of FANCF suppresses cell proliferation, migration, invasion, and drug resistance potential of breast cancer cells

Zhao, Li; Li, N.; Yu, Juan‐Han; Tang, Hong-Tao; Li, Y.L.; He, Miao; Yu, Zhaojin; Bai, Xue; Zheng, Zhaohui; Wang, E.H.

doi:10.1590/1414-431x20132938

Cited by 15 publications

(15 citation statements)

References 36 publications

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“…In the current study, an in vivo rabbit model of MI/R was established using protocols described in previous studies ( 40 , 41 ). Subsequently, the activities of SOD, LDH, CK-MB, MDA and troponin I/T in serum samples from each treatment group were evaluated.…”

Section: Discussionmentioning

confidence: 99%

Rosuvastatin relieves myocardial ischemia/reperfusion injury by upregulating PPAR‑γ and UCP2

2018

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The present study aimed to investigate whether pretreatment with rosuvastatin (RS) can provide cardioprotection in a myocardial ischemia/reperfusion (MI/R) model. The protective effect of RS on myocardial oxygen-glucose deprivation/reperfusion (OGD/R) injury was also evaluated by upregulating peroxisome proliferator-activated receptor-γ (PPAR-γ). In the present study, MI/R model was established and activities of superoxide dismutase (SOD), lactate dehydrogenase (LDH), creatine kinase-muscle/brain (CK-MB), malondialdehyde (MDA), and troponin I/T were measured. The infarct size was measured using Evans blue staining and cell viability was measured by MTT assay. Reactive oxygen species (ROS) levels were assessed by flow cytometry. Caspase-9, cytochrome c (cyt c), mitochondrial uncoupling protein 2 (UCP2) and PPAR-γ expression levels were detected by reverse transcription-quantitative polymerase chain reaction and western blotting. The results indicated that RS increased SOD activity, and decreased LDH, CK-MB, MDA and troponin I/T activities. The effect of RS was reversed by atractyloside (ATR). RS inhibited myocardial infarct size, downregulated expression of caspase-9 and cyt c and upregulated expression of UCP2 and PPAR-γ by inhibiting ATR. Furthermore, the results indicated that RS promoted cardiomyocyte viability, inhibited LDH release, reduced ROS production, decreased expression of caspase-9 and cyt c, and increased expression of UCP2 and PPAR-γ following OGD/R damage. Therefore, the present study demonstrated that RS protects primary myocardial cells against OGD/R injury by regulating PPAR-γ and UCP2. RS may be a promising therapeutic agent for treatment of MI/R injury.

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Section: Discussionmentioning

confidence: 99%

Rosuvastatin relieves myocardial ischemia/reperfusion injury by upregulating PPAR‑γ and UCP2

2018

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“…In contrast, down-regulation of miR-29a promoted the invasion of oral squamous cell carcinoma cells and tumor cell resistance [16]. Zhao et al found that inhibition of Fanconi anemia complementation group F protein increased the sensitivity of breast cancer cells to doxorubicin and resulted in decreased migration and invasion of tumor cells [17]. The epithelial mesenchymal transition (EMT) was also reported to be associated with drug resistance [17].…”

Section: Discussionmentioning

confidence: 99%

Overexpression of P16 reversed the MDR1-mediated DDP resistance in the cervical adenocarcinoma by activating the ERK1/2 signaling pathway

et al. 2019

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Background To investigate the role of P16 (INK4a)-extracellular signal related kinase 1/2 (ERK1/2) signaling pathway in cisplatin (DDP) resistance induced by multidrug resistance protein 1 (MDR1), also known as P-glycoprotein (P-gp), in cervical adenocarcinoma. Methods A human DDP-resistant HeLa cell line (HeLa/DDP) was constructed using the combination of incremental and intermittent administration of DDP. Cell Counting Kit-8 (CCK-8) assay was used to measure the IC50 and resistance index (RI) of cells. The morphological changes and population doubling time were observed under an inverted microscope. Plate cloning formation assay was performed to evaluate the cell proliferation and tumorigenic ability. Cell invasion and migration were determined by transwell assays. Besides, the expression of P16, phosphorylated extracellular signal related kinase 1 and 2 (pERK1/2), total ERK1/2 and MDR1 were measured using western blot analysis. The ERK-specific inhibitor U0126 and agonist TPA was used to explore the role of ERK. Results The DDP-resistant cervical adenocarcinoma HeLa/DDP cell line was successfully established, which showed stronger cell growth, invasion, and migration. In the HeLa/DDP cells, pERK1/2 was downregulated, P-gp was upregulated and P16 was downregulated. Overexpression of P16 led to a significant decrease in the proliferation rate, migration ability, and invasion ability of the HeLa/DDP cells. Furthermore, overexpression of P16 increased and the decreased expression of pERK1/2 and P-gp in the HeLa/DDP cells, respectively. Treatment of HeLa/DDP cells transfected with P16 plasmid with ERK-specific inhibitor U0126 significantly decreased the expression of pERK1/2 and increased the expression of P-gp from 6 h to 48 h. Moreover, after 72 h, the expression of pERK1/2 was up-regulated and the expression of P-gp was inhibited. Conclusion Overexpression of P16 could partially reverse the MDR1-mediated DDP resistance in the cervical adenocarcinoma by the enhancement of phosphorylation of ERK signaling pathway, which provided a theoretical basis for the treatment of DDP resistance in cervical adenocarcinoma. Electronic supplementary material The online version of this article (10.1186/s13008-019-0048-6) contains supplementary material, which is available to authorized users.

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“…[5] Anti-inflammatory properties of statins in the treatment or prevention of PAH in patients with COPD were also highlighted. [91417] The beneficial effects of stains are also highlighted in a systematic review and meta-analysis of observational studies that emphasized a clear benefit of statins for patients suffering from COPD. [18] An in vitro study has shown that by inhibiting 3-hydroxy-3-methylglutaryl coenzyme A reductase, atorvastatin lowered concentrations of several inflammatory molecules including IL-6 derived from basal-state endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

“…This may be an important anti-inflammatory property of statins in the treatment or prevention of PAH in patients with COPD. [9]…”

Section: Introductionmentioning

confidence: 99%

Trial of atorvastatin on serum interleukin-6, total antioxidant capacity, c-reactive protein, and alpha-1 antitrypsin in patients with chronic obstructive pulmonary disease

et al. 2018

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Objective:The present study was designed to investigate the effects of atorvastatin on serum high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), total antioxidant capacity (TAC), and alpha-1 antitrypsin (AAT) in patients with chronic obstructive pulmonary disease (COPD).Methods:A clinical trial study conducted on 42 cases of COPD (Vali-Asr Hospital, Birjand, East of Iran, years 2014–16). Patients were randomly assigned to 21 controls and 21 cases who treated with atorvastatin (40 mg/day for 6 months). Inhaled corticosteroid and long-acting β-agonist were administrated in both groups. The trial was registered at the Iranian Registry of Clinical Trials (registration number: IRCT2016042527594N1). TAC was measured by ferric reducing/antioxidant power assay. An enzyme-linked immunosorbent assay was used to determine IL-6, AAT, and hs-CRP. Spearman's rho test and Wilcoxon, Mann–Whitney, paired, and independent t-tests were used for data analysis in SPSS 23. P < 0.05 was considered significant.Findings:A number of patients completed the study were 16 in atorvastatin and 18 in control group. Mean increments (μmol/L) of TAC (mean ± standard deviation [SD]) were 12.81 ± 605.25 (P = 0.68) in atorvastatin and 160.26 ± 280.54 (P = 0.14) in control group. Mean decrements of IL-6, CRP, and AAT (mean ± SD) were 1.41 ± 5.51 (P = 0.71), 0.98 ± 5.68 (P = 0.72), and 10.94 ± 46.83 (P = 0.21) in atorvastatin and 0.91 ± 11.70 (P = 0.75), 3.23 ± 7.00 (P = 0.19), and 18.77 ± 55.90 (P = 0.21) in control group.Conclusion:Atorvastatin did not succeed in maintaining TAC and CRP reduction. However, less reduction in AAT and more reduction in IL-6 in the atorvastatin group would be likely a beneficial effect in COPD.

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RNAi-mediated knockdown of FANCF suppresses cell proliferation, migration, invasion, and drug resistance potential of breast cancer cells

Cited by 15 publications

References 36 publications

Rosuvastatin relieves myocardial ischemia/reperfusion injury by upregulating PPAR‑γ and UCP2

Rosuvastatin relieves myocardial ischemia/reperfusion injury by upregulating PPAR‑γ and UCP2

Overexpression of P16 reversed the MDR1-mediated DDP resistance in the cervical adenocarcinoma by activating the ERK1/2 signaling pathway

Trial of atorvastatin on serum interleukin-6, total antioxidant capacity, c-reactive protein, and alpha-1 antitrypsin in patients with chronic obstructive pulmonary disease

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