BTF3 confers oncogenic activity in prostate cancer through transcriptional upregulation of Replication Factor C

Zhang, Yuan; Gao, Xiang; Yi, Jingyan; Sang, Xiaolin; Dai, Zhihong; Zhou, Tao; Wang, Min; Shen, Limeng; Jia, Yaxun; Daqing, Xie; Cheng, Hai‐Ling Margaret; Liu, Zhiyu; Liu, Pixu

doi:10.1038/s41419-020-03348-2

Cited by 17 publications

(10 citation statements)

References 44 publications

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“…On the second day, ethanol was removed by centrifugation at 1500 rpm for 5 minutes. Then cells were dyed with 150 μ l working solution (50 mg/ml propidium iodide, 0.1 mg/ml RNase, and 0.2% Triton X-100) at 4°C for 30 minutes under dark conditions [ 22 ]. The cell cycle was analyzed using a flow cytometer (A00-1-1102, Beckman).…”

Section: Methodsmentioning

confidence: 99%

Inhibition of miR‐182‐5p Targets FGF9 to Alleviate Osteoarthritis

Sun

et al. 2023

Analytical Cellular Pathology

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Background. The pathogenesis of osteoarthritis (OA) is complex and there is no specific drug for treatment. The aim of this study was to identify the molecular targets of OA therapy, focusing on the expression and biological functions of miR-182-5p and its target genes in OA. Methods. miR-182-5p and fibroblast growth factor 9 (FGF9) were overexpressed or knocked down in IL-1β-induced chondrocytes. An OA knee model was performed by surgically destroying the medial meniscus. The gene expression of miR-182-5p and FGF9 was calculated. The protein FGF9 was tested by western blotting. Cell counting kit-8 (CCK8), plate cloning assay, and flow cytometry were conducted to evaluate cell proliferation and apoptosis. The expression of inflammatory factors, tumor necrosis factor-alpha (TNF-α), interleukin (IL)-6, and interleukin (IL)-8, was evaluated using enzyme-linked immunosorbent assay (ELISA). Dual-luciferase reporter assays validated the targeting relationship between miR-182-5p and FGF9. Hematoxylin–eosin (HE) and safranin O-fast Green (S–O) staining were utilized to access cartilage damage. Ki67 expression in cartilage was detected using immunohistochemistry (IHC). TdT-mediated dUTP nick-end labeling (TUNEL) assays were used to calculate the apoptosis rate of cartilage. Results. The expression of miR-182-5p was upregulated, and FGF9 was downregulated in the IL-1β-induced chondrocytes. OA chondrocytes proliferation ability in the miR-182-5p mimics group was decreased, and the apoptosis rate and inflammatory factor were increased. Transfection with miR-182-5p inhibitor increased the proliferative ability and decreased the apoptosis rate in the IL-1β-induced chondrocytes. Transfection with miR-182-5p inhibitor reversed IL-1β-induced inflammatory factor release in chondrocytes. Targeted binding sites existed between miR-182-5p and FGF9. After overexpression of FGF9, the miR-182-5p effect on OA chondrocytes was reversed. The hyaline cartilage thickness and proteoglycan content decreased in OA rats, and this was reversed by miR-182-5p inhibitor treatment. Conclusions. miR-182-5p expression levels were increased in OA chondrocytes and regulated chondrocyte proliferation, apoptosis, and inflammation by targeting FGF9. miR-182-5p is a potential gene for OA treatment.

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Section: Methodsmentioning

confidence: 99%

Inhibition of miR‐182‐5p Targets FGF9 to Alleviate Osteoarthritis

Sun

et al. 2023

Analytical Cellular Pathology

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“…DNA damage was assayed by a comet assay ( 16 ). Using alkaline lysis buffer, the cells were lysed and electrophoresed (buffer counteracted with PBS), stained, and assessed with Gold View (Coolaber, SL2140).…”

Section: Methodsmentioning

confidence: 99%

Salvia chinensis Benth Inhibits Triple-Negative Breast Cancer Progression by Inducing the DNA Damage Pathway

Wang

Han

et al. 2022

Front. Oncol.

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ObjectiveTriple-negative breast cancer (TNBC) is distinguished by early recurrence and metastases, a high proclivity for treatment resistance, and a lack of targeted medicines, highlighting the importance of developing innovative therapeutic techniques. Salvia chinensis Benth (SCH) has been widely studied for its anticancer properties in a variety of cancers. However, its significance in TNBC treatment is rarely discussed. Our study investigated the anticancer effect of SCH on TNBC and the underlying mechanisms.MethodsFirst, we used clonogenic, cell viability, flow cytometry, and Transwell assays to assess the effect of SCH on TNBC. Bioinformatic studies, especially network pharmacology-based analysis and RNA sequencing analysis, were performed to investigate the constituents of SCH and its molecular mechanisms in the suppression of TNBC. High-performance liquid chromatography and thin-layer chromatography were used to identify two major components, quercetin and β-sitosterol. Then, we discovered the synergistic cytotoxicity of quercetin and β-sitosterol and assessed their synergistic prevention of cell migration and invasion. Breast cancer xenografts were also created using MDA-MB-231 cells to test the synergistic therapeutic impact of quercetin and β-sitosterol on TNBC in vivo. The impact on the DNA damage and repair pathways was investigated using the comet assay and Western blot analysis.ResultsOur findings showed that SCH decreased TNBC cell growth, migration, and invasion while also inducing cell death. We identified quercetin and β-sitosterol as the core active components of SCH based on a network pharmacology study. According to RNA sequencing research, the p53 signaling pathway is also regarded as a critical biological mechanism of SCH treatment. The comet assay consistently showed that SCH significantly increased DNA damage in TNBC cells. Our in vivo and in vitro data revealed that the combination of quercetin and β-sitosterol induced synergistic cytotoxicity and DNA damage in TNBC cells. In particular, SCH particularly blocked the inter-strand cross-link repair mechanism and the double-strand breach repair caused by the homologous recombination pathway, in addition to inducing DNA damage. Treatment with quercetin and β-sitosterol produced similar outcomes.ConclusionThe current study provides novel insight into the previously unknown therapeutic potential of SCH as a DNA-damaging agent in TNBC.

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“…FPKM (Fragments Per Kilobase Million) were considered to estimate the gene expression level [ 20 ]. DESeq2 was applied to determine differential expression in the digital gene expression data.…”

Section: Methodsmentioning

confidence: 99%

Analysis of gene expression profiles in two spinal cord injury models

Yuan

Zhang

Zhang³

et al. 2022

Eur J Med Res

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Objectives To analyze the changes of gene expression at different timepoints after spinal cord injury (SCI) with tenth segment thoracic injury. Methods Two SCI models, the complete paraplegia (H) and Allen’s strike (D) methods were applied to induce SCI in rats, and transcriptome sequencing was performed 1, 3, 7, 14, 56, and 70 days after SCI, respectively. Principal component analysis, differentially expressed gene analysis, and hierarchical clustering analysis were applied to analyze the differentially expressed genes (DEGs). Gene Ontology GO enrichment analysis, Kyoto Encyclopedia of Genes and Genomes enrichment analysis, and Gene Set Enrichment Analysis revealed the pathway of gene enrichment. Results There were 1,907, 3,120, 3,728, 978, 2,319, and 3,798 DEGs in the complete paraplegia group and 2,380, 878, 1,543, 6,040, 1,945, and 3,850 DEGs in the Allen’s strike method group and after SCI at 1, 3, 7, 14, 56, and 70 days, respectively. The transcriptome contours of D1, H1, D3, and H14 were clustered with C; the H56, D56, H70, and D70 transcriptome contours were similar and clustered together. H3, D7, and H7 were clustered together, and D14 was clustered separately. The transcriptome differences of the two SCI models were mainly concentrated during the first 2 weeks after SCI. The DEGs after SCI in the complete paraplegia group were more concentrated. Most of the early transcriptional regulation stabilized within 2 weeks after injury. Conclusions There were DEGs between the two SCI models. Through the gene changes and pathway enrichment of the entire time period after SCI, the molecular mechanism of SCI repair was revealed in depth, which provided a reference for SCI treatment in the future.

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BTF3 confers oncogenic activity in prostate cancer through transcriptional upregulation of Replication Factor C

Cited by 17 publications

References 44 publications

Inhibition of miR‐182‐5p Targets FGF9 to Alleviate Osteoarthritis

Inhibition of miR‐182‐5p Targets FGF9 to Alleviate Osteoarthritis

Salvia chinensis Benth Inhibits Triple-Negative Breast Cancer Progression by Inducing the DNA Damage Pathway

Analysis of gene expression profiles in two spinal cord injury models

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