Cleaved PARP‐1, an Apoptotic Marker, can be Detected in Ram Spermatozoa

Casao, A.; Mata-Campuzano, M.; Ordás, L.; Cebrián‐Pérez, J. A.; Muiño‐Blanco, T.; Martínez‐Pastor, Felipe

doi:10.1111/rda.12549

Cited by 20 publications

(15 citation statements)

References 20 publications

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“…It is shown that COX-2 was inhibited by caspase-3 after irradiation, and the inhibition of COX-2 could sensitize cancer cells to apoptosis [22,23]. RAPR is another important substrate of caspase-3, in which it is decomposed to an 85-kDa product, cRAPR, that can be identified as an apoptotic marker [24][25][26].…”

Section: Introductionmentioning

confidence: 99%

α-bisabolol enhances radiotherapy-induced apoptosis in endometrial cancer cells by reducing the effect of XIAP on inhibiting caspase-3

Fang¹,

Wang²,

Li³

et al. 2019

Bioscience Reports

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Endometrial cancer (EC) is one of the most common cancers in females. Although the diagnosis and treatment in early stages can greatly improve the survival rate of patients, the advanced EC still is lethal. Radiotherapy is widely used against EC, and it is a great challenge to find an effective way to overcome the resistance of EC during radiotherapy. α-bisabolol is a promising drug, which has already exhibited its anti-tumor effect in some malignancies. Here we reported that α-bisabolol could inhibit the proliferation of EC cells. It is also shown that their abilities of migration and invasion were effectively reduced by α-bisabolol. Furthermore, our results also demonstrated that α-bisabolol could improve sensitivity of EC cells in radiotherapy and further inhibited the growth of EC cells. By Western blot, we found the expression of matrix metalloproteinases-9 (MMP-9) and cyclin E were significantly decreased, which indicated that EC cells can be further suppressed by using α-bisabolol and radiotherapy. It is also demonstrated in our study that the rate of apoptotic cells is markedly increased in EC by using these two treatments. The significant decrease in X-linked inhibitor of apoptosis protein (XIAP) and increase in caspase-3 detected in our study suggested that the enhancement of apoptosis is mediated by XIAP/caspase-3 pathway, which was further confirmed by examining the downstream effectors of caspase-3, COX-2, PARP and cleaved PARP. In the present study, we demonstrated that α-bisabolol could enhance the sensitivity of EC cells to radiotherapy, which provide a novel alternative for overcoming radioresistance of EC cells and achieving a better outcome in radiotherapy.

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Section: Introductionmentioning

confidence: 99%

α-bisabolol enhances radiotherapy-induced apoptosis in endometrial cancer cells by reducing the effect of XIAP on inhibiting caspase-3

Fang¹,

Wang²,

Li³

et al. 2019

Bioscience Reports

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“…HaCaT cells showed decreasing cell viability and increasing apoptosis after LPS treatment, which indicated that LPS brought great effects in cell growth. In addition, cleaved-PARP, cleaved-caspase-3 and cleaved-caspase-9 are three crucial factors [30][31][32]. Western blot results demonstrated that these three factors are all positively regulated by LPS and down-regulated by emodin, which validated the inhibitory effects of emodin on apoptosis.…”

Section: Discussionmentioning

confidence: 67%

Emodin protects against lipopolysaccharide-induced inflammatory injury in HaCaT cells through upregulation of miR-21

Song

Cui

Zhao

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Background/aim: Pressure ulcers are a disastrous health issue in which inflammation is involved. Emodin possesses biological properties in inflammation. Our study investigated functions of emodin in lipopolysaccharide (LPS)-treated HaCaT cells. Methods: LPS was used to induce cell inflammation. MTT and flow cytometry were applied for cell viability and apoptosis assays, respectively. Moreover, apoptotic proteins were detected by western blot. Similarly, inflammatory factors and signalling related proteins were also determined by western blot. Results: Emodin increased cell viability and diminished apoptosis in LPS-treated HaCaT cells. Moreover, cleaved-PARP, cleaved-caspase-3 and cleaved-caspase-9 were all downregulated by emodin. Furthermore, inflammatory factors IL-1b, IL-6, Cox-2 and iNOS were inhibited by emodin in LPS-treated cells. In addition, emodin decreased phosphorylation of p65 and IjBa and the level of PTEN while enhanced phosphorylation of PI3K and AKT. Importantly, emodin increased expression of miR-21 suppressed by LPS and miR-21 downregulation negated the protective functions of emodin. Conclusions: Emodin promoted cell growth presented by increasing viability and blocking apoptosis process with inflammation inhibition. The protective activity of emodin was mediated by miR-21 up-regulation.

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“…PARP serves an important role in the repair of damaged DNA caused by a variety of cellular stresses (38). Also, cleaved PARP (~89 kDa) is known as a marker for apoptotic cell death (39). Therefore, PARP cleavage by PB irradiation was explored to determine whether Capan-1 cell death by PB was due to apoptosis.…”

Section: Resultsmentioning

confidence: 99%

The association of changes in RAD51 and survivin expression levels with the proton beam sensitivity of Capan‑1 and Panc‑1 human pancreatic cancer cells

Lee

Nam

2018

Int J Oncol

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Fewer than 20% of patients diagnosed with pancreatic cancer can be treated with surgical resection. The effects of proton beam irradiation were evaluated on the cell viabilities in Panc-1 and Capan-1 pancreatic cancer cells. The cells were irradiated with proton beams at the center of Bragg peaks with a 6-cm width using a proton accelerator. Cell proliferation was assessed with the MTT assay, gene expression was analyzed with semi-quantitative or quantitative reverse transcription-polymerase chain reaction analyses and protein expression was evaluated by western blotting. The results demonstrated that Capan-1 cells had lower cell viability than Panc-1 cells at 72 h after proton beam irradiation. Furthermore, the cleaved poly (ADP-ribose) polymerase protein level was increased by irradiation in Capan-1 cells, but not in Panc-1 cells. Additionally, it was determined that histone H2AX phosphorylation in the two cell lines was increased by irradiation. Although a 16 Gy proton beam was only slightly up-regulated cyclin-dependent kinase inhibitor 1 (p21) protein expression in Capan-1 cells, p21 expression levels in Capan-1 and Panc-1 cells were significantly increased at 72 h after irradiation. Furthermore, it was observed that the expression of DNA repair protein RAD51 homolog 1 (RAD51), a homogenous repair enzyme, was decreased in what appeared to be a dose-dependent manner by irradiation in Capan-1 cells. Contrastingly, the transcription of survivin in Panc-1 was significantly enhanced. The results suggest that RAD51 and survivin are potent markers that determine the therapeutic efficacy of proton beam therapy in patients with pancreatic cancer.

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Cleaved PARP‐1, an Apoptotic Marker, can be Detected in Ram Spermatozoa

Cited by 20 publications

References 20 publications

α-bisabolol enhances radiotherapy-induced apoptosis in endometrial cancer cells by reducing the effect of XIAP on inhibiting caspase-3

α-bisabolol enhances radiotherapy-induced apoptosis in endometrial cancer cells by reducing the effect of XIAP on inhibiting caspase-3

Emodin protects against lipopolysaccharide-induced inflammatory injury in HaCaT cells through upregulation of miR-21

The association of changes in RAD51 and survivin expression levels with the proton beam sensitivity of Capan‑1 and Panc‑1 human pancreatic cancer cells

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