Silencing of <scp>JMJD2B</scp> induces cell apoptosis via mitochondria‐mediated and death receptor‐mediated pathway activation in colorectal cancer

Sun, Bei; Fu, Lin; Wang, Yun Qian; Gao, Qin; Xu, Jie; Zhi, Cao; Chen, Ying Xuan; Fang, Jing

doi:10.1111/1751-2980.12166

Cited by 24 publications

(23 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The role of JMJD2A in cancer cellular proliferation is also verified via JMJD2A silencing in osteosarcoma cells [16]. The oncogenetic features of JMJD2B have been reported in colorectal cancer [17], gastric cancer [18], breast cancer [19], and so on. The oncogenetic features of JMJD2C have been reported in the progression of breast cancer [20] and colon cancer [11].…”

Section: Introductionmentioning

confidence: 86%

Histone demethylase JMJD2B and JMJD2C induce fibroblast growth factor 2: mediated tumorigenesis of osteosarcoma

Dong

2015

Med Oncol

View full text Add to dashboard Cite

JMJD2B and JMJD2C, histone demethylases, play crucial roles in cancer development and are up-regulated in many cancers. However, the actions of JMJD2B and JMJD2C in osteosarcoma remain unknown. The levels of JMJD2B or JMJD2C were evaluated in osteosarcoma cells and tissues via quantitative real-time PCR and Western Blot. JMJD2B and JMJD2C were up-regulated in osteosarcoma tissues when compared to paired adjacent non-tumor tissues. A higher level of JMJD2B or JMJD2C was related with metastasis of osteosarcoma cells. Fibroblast growth factor 2 (FGF2) is an important factor to maintain immaturity of cells and contributes to osteosarcoma aggressiveness. Elevated levels of FGF2 promoted the proliferation, migration, and invasion of osteosarcoma cell, while FGF2 was up-regulated by JMJD2B or JMJD2C. GST pull-down assay showed that JMJD2B or JMJD2C interacted with FGF2. Thus, JMJD2B and JMJD2C play an important role in the pathology of osteosarcoma via the up-regulation of FGF2. JMJD2B and JMJD2C should be developed potential targets for the therapy of osteosarcoma patients.

show abstract

Section: Introductionmentioning

confidence: 86%

Histone demethylase JMJD2B and JMJD2C induce fibroblast growth factor 2: mediated tumorigenesis of osteosarcoma

Dong

2015

Med Oncol

View full text Add to dashboard Cite

show abstract

“…As a member of the histone demethylase family, KDM4B was reported to correlate with proliferation and metastasis in prostate cancer, colorectal cancer and gastric cancer [12][13][14]. However, its role in pancreatic cancer has seldom been reported.…”

Section: Introductionmentioning

confidence: 99%

KDM4B promotes epithelial-mesenchymal transition through up-regulation of ZEB1 in pancreatic cancer

Li¹,

Wu²,

Wang³

et al. 2015

ABBS

View full text Add to dashboard Cite

Lysine (K)-specific demethylase 4B (KDM4B) is a histone H3K9 demethylase and is reported to activate gene transcription through regulation of chromatin structures. Previous research has revealed that KDM4B plays special regulatory roles in colorectal, prostate and gastric cancers. However, its physiological role in pancreatic cancer remains largely unknown. In the present study, it is demonstrated KDM4B plays a crucial in epithelial-mesenchymal transition (EMT) in pancreatic cancer. siRNA mediated silencing of KDM4B inhibits cell migration, invasion and EMT. Moreover, KDM4B was demonstrated to epigenetically regulate the expression of ZEB1 in the TGF-β-induced EMT process. In tumor tissues of pancreatic cancer patient, the protein level of KDM4B was positively correlated with ZEB1. In conclusion, our results suggested that KDM4B is a key mediator in EMT process, and may serve as an important prognostic marker and therapeutic target for the metastatic progression of human pancreatic cancer.

show abstract

“…65,66 As mentioned previously, HDACIs activate the mitochondrial apoptotic pathway by releasing cytochrome c from the mitochondrial intermembrane space and activating caspase-3. 67 Therefore, to further characterize the specific apoptotic pathways activated by TUB-A and PdNPs, we measured caspase-3 activity in cells that were subjected to single or combined drug treatment for 24 h, in the presence or absence of a caspase-3 inhibitor. The combination of TUB-A and PdNPs induced a significantly higher level of caspase-3 activity than did the single-drug treatments.…”

mentioning

confidence: 99%

Combination of palladium nanoparticles and tubastatin-A potentiates apoptosis in human breast cancer cells: a novel therapeutic approach for cancer

Yuan¹,

Peng²,

Gurunathan³

2017

IJN

View full text Add to dashboard Cite

Background Breast cancer is the most common malignant disease that occurs in women. Histone deacetylase (HDAC) inhibition has recently emerged as an effective and attractive target for the treatment of cancer. The aim of this study was to investigate the efficacy of a combined treatment of tubastatin A (TUB-A) and palladium nanoparticles (PdNPs) against MDA-MB-231 human breast cancer cells using two different cytotoxic agents that work by two different mechanisms, thereby decreasing the probability of chemoresistance in cancer cells and increasing the efficacy of toxicity, to provide efficient therapy for advanced stage of cancer without any undesired side effects. Methods PdNPs were synthesized using a novel biomolecule called R-phycoerythrin and characterized using various analytical techniques. The combinatorial effect of TUB-A and PdNPs was assessed by various cellular and biochemical assays and also by gene expression analysis. Results The biologically synthesized PdNPs had an average size of 25 nm and were spherical in shape. Treatment of MDA-MB-231 human breast cancer cells with TUB-A or PdNPs showed a dose-dependent effect on cell viability. The combination of 4 μM TUB-A and 4 μM PdNPs had a significant inhibitory effect on cell viability compared with either TUB-A or PdNPs alone. The combinatorial treatment also had a more pronounced effect on the inhibition of HDAC activity and enhanced apoptosis by regulating various cellular and biochemical changes. Conclusion Our results suggest that there was a strong synergistic interaction between TUB-A and PdNPs in increasing apoptosis in human breast cancer cells. These data provide an important preclinical basis for future clinical trials on this drug combination. This combinatorial treatment increased therapeutic potentials, thereby demonstrating a relevant targeted therapy for breast cancer. Furthermore, we have provided the first evidence for the combinatorial effect and mechanism of toxicity of TUB-A and PdNPs in human breast cancer cells. The novelties of the study were identification of a combination therapy that consists of suitable therapeutic molecules that kill cancer cells and also exploration of two different possible mechanisms involved to reduce chemoresistance in cancer cells.

show abstract

Silencing of JMJD2B induces cell apoptosis via mitochondria‐mediated and death receptor‐mediated pathway activation in colorectal cancer

Abstract: JMJD2B silencing induced CRC cell apoptosis via both mitochondria-related and death receptor-related pathways. The cleavage of Bid activated by caspase-8 might serve as a crosstalk mediator between these two pathways in CRC.

Cited by 24 publications

References 22 publications

Histone demethylase JMJD2B and JMJD2C induce fibroblast growth factor 2: mediated tumorigenesis of osteosarcoma

Histone demethylase JMJD2B and JMJD2C induce fibroblast growth factor 2: mediated tumorigenesis of osteosarcoma

KDM4B promotes epithelial-mesenchymal transition through up-regulation of ZEB1 in pancreatic cancer

Combination of palladium nanoparticles and tubastatin-A potentiates apoptosis in human breast cancer cells: a novel therapeutic approach for cancer

Contact Info

Product

Resources

About