Poly (ADP‐ribose) polymerase‐1 binds to BCL2 major breakpoint region and regulates BCL2 expression

Yang, Nan; Gong, Fei‐Ran; Sun, Luan; Yang, Da‐Peng; Han, Xiao; Ma, Castello; Sun, Yujie

doi:10.1002/jcb.22635

Cited by 8 publications

(6 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Since gene regulation occurs at different levels it is possible that PARP-1 affects Bcl-2 expression both at transcriptional or post-transcriptional level [65]. Recently, Dutta et al [66] have demonstrated that Bcl-2 may influence PARP activity both in vitro and in cancer cells by a direct interaction with PARP-1.…”

Section: Discussionmentioning

confidence: 99%

PARP-1 Modulates Amyloid Beta Peptide-Induced Neuronal Damage

et al. 2013

View full text Add to dashboard Cite

Amyloid beta peptide (Aβ) causes neurodegeneration by several mechanisms including oxidative stress, which is known to induce DNA damage with the consequent activation of poly (ADP-ribose) polymerase (PARP-1). To elucidate the role of PARP-1 in the neurodegenerative process, SH-SY5Y neuroblastoma cells were treated with Aβ25–35 fragment in the presence or absence of MC2050, a new PARP-1 inhibitor. Aβ25–35 induces an enhancement of PARP activity which is prevented by cell pre-treatment with MC2050. These data were confirmed by measuring PARP-1 activity in CHO cells transfected with amylod precursor protein and in vivo in brains specimens of TgCRND8 transgenic mice overproducing the amyloid peptide. Following Aβ25–35 exposure a significant increase in intracellular ROS was observed. These data were supported by the finding that Aβ25–35 induces DNA damage which in turn activates PARP-1. Challenge with Aβ25–35 is also able to activate NF-kB via PARP-1, as demonstrated by NF-kB impairment upon MC2050 treatment. Moreover, Aβ25–35 via PARP-1 induces a significant increase in the p53 protein level and a parallel decrease in the anti-apoptotic Bcl-2 protein. These overall data support the hypothesis of PARP-1 involvment in cellular responses induced by Aβ and hence a possible rationale for the implication of PARP-1 in neurodegeneration is discussed.

show abstract

Section: Discussionmentioning

confidence: 99%

PARP-1 Modulates Amyloid Beta Peptide-Induced Neuronal Damage

et al. 2013

View full text Add to dashboard Cite

show abstract

“…Tumor–bone molecular interactions mediated by various factors drive a cycle that perpetuates skeletal metastases 39 . Breast cancer cells produce various osteolytic mediators, of which IL-8 and PTHrP cause bone destruction by inducing the differentiation and activation of osteoclasts 40 . Our data showed that expressions of both IL-8 and PTHrP were increased by Osx overexpression, thus enhancing osteoclast activity.…”

Section: Discussionmentioning

confidence: 99%

“…ChIP assays were accomplished as described previously 40 . Briefly, formaldehyde cross-linking was performed in MDA-MB 231 cells, and the resulting samples were sonicated to shear cross-linked chromatin.…”

Section: Methodsmentioning

confidence: 99%

Upregulated osterix promotes invasion and bone metastasis and predicts for a poor prognosis in breast cancer

Yao

Wang

et al. 2019

Cell Death Dis

Self Cite

View full text Add to dashboard Cite

Approximately 70% of patients with advanced breast cancer develop bone metastases, accompanied by complications, such as bone pain, fracture, and hypercalcemia. However, our understanding of the molecular mechanisms that govern this process remains fragmentary. Osterix (Osx) is a zinc finger-containing transcription factor essential for osteoblast differentiation and bone formation. Here, we identified the functional roles of Osx in facilitating breast cancer invasion and bone metastasis. Osx upregulation was associated with lymph node metastasis and was negatively prognostic for overall survival. Knockdown of Osx inhibited invasion of breast cancer and osteolytic metastasis by downregulating MMP9, MMP13, VEGF, IL-8, and PTHrP, which are involved in invasion, angiogenesis, and osteolysis; overexpression of Osx had the opposite effect. Moreover, MMP9 was a direct target of Osx and mediated the Osx-driven invasion of breast cancer cells. Together, our data showed that Osx facilitates bone metastasis of breast cancer by upregulating the expression of a cohort of genes that contribute to steps in the metastatic cascade. These findings suggest that Osx is an attractive target for the control of bone metastasis of breast cancers.

show abstract

“…ChIP assays were performed as described previously [29]. The protein-DNA complexes were immunoprecipitated using anti-TCN1 antibody (ab202121, Abcam), anti-ITGB4 antibody (ab182120, Abcam) or immunoglobulin G (IgG, ab172730, Abcam), which served as a control.…”

Section: Chromatin Immunoprecipitation (Chip) Assaysmentioning

confidence: 99%

TCN1 Deficiency Inhibits The Malignancy of Colorectal Cancer Cells By Regulating The ITGB4 Pathway

Zhu

Jiang

Huang

et al. 2021

Preprint

View full text Add to dashboard Cite

Background: This study aimed to investigate the biological function and regulatory mechanism of TCN1 in colorectal cancer (CRC). Methods: We studied the biological functions of TCN1 using gain-of-function and loss-of-function analysis in HCT116 cell lines, and examined the effects of TCN1 on the proliferation, apoptosis, and invasion of CRC cells and determined its potential molecular mechanisms using CRC lines and mouse xenotransplantation models. Tumor xenograft and tumor metastasis studies were performed to detect the tumorigenicity and metastasis of cells in vivo. Results: TCN1-knockdown attenuated CRC cell proliferation, invasion and promoted cell apoptosis. Overexpression of TCN1 yielded the opposite effects. In addition, TCN1-knockdown HCT116 cells failed to form metastatic foci in the peritoneum after intravenous injection. Molecular mechanism studies showed that TCN1 interacts with integrin subunit β4 (ITGB4) to positively regulate the expression of ITGB4. TCN1-knockdown promoted the degradation of ITGB4 and increased the instability of ITGB4 and filamin A (FLNA). Downregulation of ITGB4 at the protein level resulted in the disassociation of the ITGB4/PLEC complex, leading to cytoskeletal damage. Conclusion: TCN1 might exert oncogenic role in CRC via regulating the ITGB4 signaling pathway.

show abstract

Poly (ADP‐ribose) polymerase‐1 binds to BCL2 major breakpoint region and regulates BCL2 expression

Cited by 8 publications

References 35 publications

PARP-1 Modulates Amyloid Beta Peptide-Induced Neuronal Damage

PARP-1 Modulates Amyloid Beta Peptide-Induced Neuronal Damage

Upregulated osterix promotes invasion and bone metastasis and predicts for a poor prognosis in breast cancer

TCN1 Deficiency Inhibits The Malignancy of Colorectal Cancer Cells By Regulating The ITGB4 Pathway

Contact Info

Product

Resources

About