Over-Expression of Telomere Binding Factors (TRF1 &amp; TRF2) in Renal Cell Carcinoma and Their Inhibition by Using SiRNA Induce Apoptosis, Reduce Cell Proliferation and Migration Invitro

Pal, Devendra; Sharma, Ujjawal; Singh, Shrawan Kumar; Kakkar, Nandita; Prasad, Rajendra

doi:10.1371/journal.pone.0115651

Cited by 39 publications

(34 citation statements)

References 21 publications

(21 reference statements)

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“…Proliferation and apoptosis are very important physiological processes for cancer cells (26). Apoptosis is an important cause of cell proliferation inhibition (8). Apoptosis (programmed cell death), is an essential mechanism through which many types of chemotherapeutic agents inhibit tumor growth (27).…”

Section: Discussionmentioning

confidence: 99%

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A novel polysaccharide derived from algae extract induces apoptosis and cell cycle arrest in human gastric carcinoma MKN45 cells via ROS/JNK signaling pathway

Xie

Fujii

Zhao³

et al. 2016

International Journal of Oncology

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In recent years, interest in biological activities of compounds from marine organisms has intensified. Cancer is the most principal enemy for human life and health. For the first time, to the best of our knowledge, we investigated a novel algae-derived polysaccharide for its role in inducing apoptosis and cell cycle arrest in human gastric carcinoma MKN45 cells. We found that the novel polysaccharide suppressed MKN45 cell proliferation, induced cell apoptosis and arrested the cells at G2/M phase. Furthermore, we observed that the generation of reactive oxygen species (ROS) and the phosphorylation of Jun N-terminal kinase (JNK), p53, caspase-9 and -3 were induced in the polysaccharide-treated MKN45 cells. In addition, pretreatment with N-acetyl-cysteine (NAC) and SP600125, the inhibitor of ROS and JNK, induced MKN45 cell proliferation, prevented the cell apoptosis and released the cells from cycle arrest. Finally, we found that pretreatment with NAC prevented the JNK, p53, caspase-9 and -3 protein phosphorylation induced by the polysaccharide, however, pretreatment with SP600125 did not affect the generation of ROS, suggesting that ROS is upstream of JNK. Taken together, the novel polysaccharide induced cancer cell apoptosis and arrested cell cycle via ROS/JNK signaling pathway.

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Section: Discussionmentioning

confidence: 99%

“…Apoptosis is an important cause of cell proliferation inhibition (8). There is compelling evidence that excessive reactive oxygen species (ROS) production surmounts cellular antioxidant defenses, triggering apoptosis (9).…”

Section: Introductionmentioning

confidence: 99%

A novel polysaccharide derived from algae extract induces apoptosis and cell cycle arrest in human gastric carcinoma MKN45 cells via ROS/JNK signaling pathway

Xie

Fujii

Zhao³

et al. 2016

International Journal of Oncology

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“…[17][18][19][20] In the present study, we first detected the miR-140 expression in human PCa tissues and cells, and a decreased miR-140 expression was confirmed in human PCa cells and tissues. [17][18][19][20] In the present study, we first detected the miR-140 expression in human PCa tissues and cells, and a decreased miR-140 expression was confirmed in human PCa cells and tissues.…”

Section: Discussionmentioning

confidence: 98%

MicroRNA‐140 inhibit prostate cancer cell invasion and migration by targeting YES proto‐oncogene 1

Zhao

Jie

et al. 2019

J of Cellular Biochemistry

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Prostate cancer (PCa), which is an aggressive malignancy of the male genitourinary system. In the present study, the effects of microRNA‐140 (miR‐140) on PCa were determined. We transfected miR‐140 mimics or negative control into PCa cells, and we used MTT, wound healing, and Transwell assays for determining the capacities of miR‐140 in cell proliferation, migration, and invasion, respectively. We also confirmed the relationship between miR‐140 and YES proto‐oncogene 1 (YES1) using Luciferase reporter assay. The results showed that miR‐140 was downregulated in PCa cells and tissues, and overexpression of miR‐140 could significantly suppress their capacities of proliferation, migration, and invasion. Moreover, YES1 was shown to be a direct target of miR‐140. Moreover, miR‐140 expression is negatively correlated with YES1 levels. miR‐140 exhibits significant tumor‐suppressive effects in PCa by inhibiting YES1. The study indicated that miR‐140 and YES1 could be the potential targets for PCa therapy.

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“…Gastric carcinomas with short telomeres expressed proeminent levels of telomerase in addition to TRF1, TRF2 and TIN2 overexpression (Matsutani et al, 2001). TRF1 and TRF2 genes, and often TIN2 gene were also found to be upregulated in adult Tcell leukemia (Bellon et al, 2006), lung cancer (Nakanishi et al, 2003), renal cell carcinoma (RCC) (Pal et al, 2015) and hepatocarcinoma (Yokota et al, 2003). However, at the moment, the carcinogenic mechanisms triggered by telomeric binding proteins (especially TRF1 and TRF2) overexpression remain elusive.…”

Section: Somatic Cells and Cancermentioning

confidence: 99%

“…Interestingly, TRF1 and TRF2 genes silencing triggered apoptosis and cell cycle arest in a RCC cell line. Thus, TRF1 and TRF2 inhibition may hold substantial promise for the attenuation of genomic instability and treatment of cancers (Pal et al, 2015).…”

Section: Somatic Cells and Cancermentioning

confidence: 99%

Telomeres and telomere dysfunctions

Dobre¹,

Dinescu²,

Costache³

2018

Rev. Biol. Biomed. Sci.

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The length of telomeres is an important determinant of cell viability and phenotype. In stem cells, telomere shortening affects their self-renewal potential and compromises the regeneration of a variety of tissues. Telomeropathies, also known as telomeres diseases or telomeres syndromes, are a suggestive example in this context. These diseases are caused by mutations in genes coding for proteins involved in telomere maintenance and repair. Telomere attrition is also a source of genomic instability. Cells that display frayed telomeres and dysfunctional tumor suppressor genes, often activate telomere maintenance mechanisms, telomerase or alternative lengthening of telomeres, and become immortal. Carcinogenesis is initiated more easily in stem cells, because they exhibit low levels of telomerase. Thus, in response to mutations induced by telomere shortening and environmental exposure, stem cells can enhance telomerase activity to stabilize their genome, gaining unlimited proliferation capacity at the same time. In this paper, we reviewed the literature on telomere biology in order to understand the molecular underpinnings of telomere maintenance and its involvement in human diseases, especially age-associated diseases and cancer.

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Over-Expression of Telomere Binding Factors (TRF1 & TRF2) in Renal Cell Carcinoma and Their Inhibition by Using SiRNA Induce Apoptosis, Reduce Cell Proliferation and Migration Invitro

Cited by 39 publications

References 21 publications

A novel polysaccharide derived from algae extract induces apoptosis and cell cycle arrest in human gastric carcinoma MKN45 cells via ROS/JNK signaling pathway

A novel polysaccharide derived from algae extract induces apoptosis and cell cycle arrest in human gastric carcinoma MKN45 cells via ROS/JNK signaling pathway

MicroRNA‐140 inhibit prostate cancer cell invasion and migration by targeting YES proto‐oncogene 1

Telomeres and telomere dysfunctions

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