Evaluation of apoptosis-associated protein (Bcl-2, Bax, cleaved caspase-3 and p53) expression in canine mammary tumors: An immunohistochemical and prognostic study

Dolka, I.; Król, Magdalena; Sapierzyński, R.

doi:10.1016/j.rvsc.2016.02.004

Cited by 108 publications

(69 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In line with our results, Lei et al also revealed that knockdown of CDR1as could work as an oncogene in HCC via the suppression of HCC cell proliferation and invasion through targeting miR‐7 . Bax/Bcl2 and cleaved‐Caspase‐3/Caspase‐3 are commonly used indicators of apoptosis . Interestingly, CDR1as up‐regulated the Caspase‐3 activity and apoptosis of cells, while overexpression of miR‐7a reversed CDR1as‐induced phenotypes, leading to decreased Caspase‐3 activity and apoptosis, which were consistent with our findings.…”

Section: Discussionsupporting

confidence: 90%

Silencing CDR1as enhances the sensitivity of breast cancer cells to drug resistance by acting as a miR‐7 sponge to down‐regulate REGγ

Yang

Xiao

Wang

et al. 2019

J Cellular Molecular Medi

View full text Add to dashboard Cite

In our study, we aimed to investigate the role of CDR1as during competitive inhibition of miR‐7 in the regulation of cisplatin chemosensitivity in breast cancer via regulating REGγ. RT‐qPCR was applied to detect the expression of CDR1as and miR‐7 in breast cancer tissues, breast cancer cell lines and corresponding drug‐resistant cell lines. The correlation between CDR1as and miR‐7 and between miR‐7 and REGγ was evaluated. MCF‐7‐R and MDA‐MB‐231‐R cells were selected followed by transfection of a series of mimics, inhibitors or siRNA. The effect of CDR1as on the half maximal inhibitor concentration (IC50), cisplatin sensitivity and cell apoptosis was also analysed. Furthermore, a subcutaneous xenograft nude mouse model was established to further confirm the effect of CDR1as on the chemosensitivity of breast cancer to cisplatin in vivo. Immunohistochemical staining was conducted to test the Ki‐67 expression in nude mice. A positive correlation was found between the drug resistance and CDR1as expression in breast cancer. CDR1as could increase the resistance of breast cancer cells to cisplatin. miR‐7 expression was low, while REGγ was highly expressed in MCF‐7‐R and MDA‐MB‐231‐R cells. CDR1as competitively inhibited miR‐7 and up‐regulated REGγ. Overexpression of miR‐7 could reverse the enhanced sensitivity of silenced CDR1as to drug‐resistant breast cancer cells. Additionally, in vivo experiments demonstrated that CDR1as mediated breast cancer occurrence and its sensitivity to cisplatin. Silencing CDR1as decreased Ki‐67 expression. Silencing CDR1as may inhibit the expression of REGγ by removing the competitive inhibitory effect on miR‐7 and thus enhancing the sensitivity of drug‐resistant breast cancer cells.

show abstract

Section: Discussionsupporting

confidence: 90%

Silencing CDR1as enhances the sensitivity of breast cancer cells to drug resistance by acting as a miR‐7 sponge to down‐regulate REGγ

Yang

Xiao

Wang

et al. 2019

J Cellular Molecular Medi

View full text Add to dashboard Cite

show abstract

“…Proteins involved in cell cycle regulation, CCND1 and CDK2/4, were all reduced after the siTRPM7 treatment. Moreover, proteins involved in apoptosis were strongly altered, especially imbalance of the BAX/BCL2 ratio, which is involved in mitochondrial-dependent apoptosis [62, 63], and related proteins including cleaved-caspase 3 [64, 65] and Cytochrome C [66, 67], suggesting that TRPM7 deficiency could trigger a mitochondrial-mediated apoptosis. Importantly, as suggested by our microarray analysis, MAPK signaling pathway, a central regulator in the pathway network, could be altered by the affected calcium signaling pathway due to TRPM7 knockdown.…”

Section: Discussionmentioning

confidence: 99%

DecreasedTRPM7inhibits activities and induces apoptosis of bladder cancer cells via ERK1/2 pathway

et al. 2016

View full text Add to dashboard Cite

Transient receptor potential melastatin 7 (TRPM7) functions as a Mg2+/Ca2+-permeable channel fused with a kinase domain and regulates various physical processes and diseases. However, its effects on pathogenesis of human bladder cancer (BCa) has not been clarified yet. Our microarray analysis has suggested that calcium signaling pathway is connected with bladder cancer via MAPK pathway. Therefore, we aim to investigate the mechanism of TRPM7 in BCa tumorigenesis by using BCa tissues compared with normal bladder epithelium tissues, as well as using distinct BCa cell lines (EJ, 5637 and T24). We observed increased TRPM7 expression and dysregulation of proteins involved in Epithelial-Mesenchymal Transition (EMT) in BCa tissues. Moreover, knockdown of TRPM7 in BCa cells reversed the EMT status, accompanied by increase of reactive oxygen species (ROS). Furthermore, TRPM7 deficiency could inhibit BCa cell proliferation, migration and invasion, as well as induce p-ERK1/2 and suppress PI3K/AKT at the protein level. Downregulation of TRPM7 promoted cell cycle arrest at G0/G1 phase and apoptosis in vitro, which could be recovered by pre-treatment with U0126 to deactivate ERK1/2, suggesting a close correlation between TRPM7 and the MAPK signaling pathway. Furthermore, a NOD/SCID mouse model transplanted using the BCa cells was established, revealing delayed tumor growth by reduced protein activity and mRNA transcription of TRPM7 in vivo. Our results suggested TRPM7 might be essential for BCa tumorigenesis by interfering BCa cell proliferation, motility and apoptosis.

show abstract

“…As well known, Bcl‐2 is an anti‐apoptotic protein, and Bax is a pro‐apoptotic protein. Caspase‐3, a member of caspases family, is cleaved during apoptosis . The results of Western blot and real‐time PCR showed that along with the increased concentration of hinokiflavone, the expression of Bcl‐2 decreased, whereas that of Bax and cleaved caspase‐3 increased (Fig.…”

Section: Resultsmentioning

confidence: 95%

Antitumor activity in colorectal cancer induced by hinokiflavone

Zhou

Zhao

et al. 2019

J of Gastro and Hepatol

View full text Add to dashboard Cite

Background and Aim Colorectal cancer is one of the most common malignant disease worldwide with highly metastatic potential. Identification of effective therapeutic treatment overcoming such disease is an urgent need. Our study focuses on hinokiflavone as an antitumor agent against colorectal cancer. Methods MTT assay, cell colony formation assay, Hoechst staining, flow cytometry, Western blot analysis, real‐time polymerase chain reaction, and migration and invasion assay were performed to identify the effects of hinokiflavone on cell proliferation, apoptosis, and metastasis. CT26 tumor‐bearing mice model was conducted to explore the antitumor activity of hinokiflavone in vivo. Immunohistochemistry staining was used to detect the protein expression of Ki‐67, cleaved caspase‐3, and MMP9 in treated tumors. Acute toxicity was evaluated by serological and hematological analyses, and drug side effect on organs was evaluated by hematoxylin and eosin staining. Results Hinokiflavone reduced the proliferation, migration, and invasion and promoted the apoptosis in colorectal tumor cells in vitro. Treatment of hinokiflavone at a tolerable and safe dose (50 mg/kg) significantly suppressed tumor growth in mice bearing CT26 tumors by reducing tumor proliferation and metastasis and inducing apoptosis. Mechanically, treatment of hinokiflavone induced apoptosis by loss of mitochondrial transmembrane potential and increased reactive oxygen species generation. Conclusions Hinokiflavone suppressed colorectal tumor cell proliferation, induced apoptosis via the reactive oxygen species–mitochondria‐mediated apoptotic pathway, and inhibited tumor cell migration and invasion. Antitumor activity of hinokiflavone was also validated in mice model without observed toxicity. Our findings suggested that the plant‐derived hinokiflavone could be used as an antitumor agent against colorectal cancer.

show abstract

Evaluation of apoptosis-associated protein (Bcl-2, Bax, cleaved caspase-3 and p53) expression in canine mammary tumors: An immunohistochemical and prognostic study

Cited by 108 publications

References 31 publications

Silencing CDR1as enhances the sensitivity of breast cancer cells to drug resistance by acting as a miR‐7 sponge to down‐regulate REGγ

Silencing CDR1as enhances the sensitivity of breast cancer cells to drug resistance by acting as a miR‐7 sponge to down‐regulate REGγ

DecreasedTRPM7inhibits activities and induces apoptosis of bladder cancer cells via ERK1/2 pathway

Antitumor activity in colorectal cancer induced by hinokiflavone

Contact Info

Product

Resources

About