A combination of STI571 and BCR-ABL1 siRNA with overexpressed p15INK4B induced enhanced proliferation inhibition and apoptosis in chronic myeloid leukemia

Xia, Dongdong; Liu, L.; Hao, Ming-Hua; Liu, Q.; Chen, R.A.; Liang, Yingmin

doi:10.1590/1414-431x20143734

Cited by 6 publications

(3 citation statements)

References 23 publications

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“…CDKN2B belongs to the INK4 protein family. The CDKN2B-encoded p15INK4B protein binds to and inhibits cyclin-dependent kinases 4 (CDK4) and cyclin-dependent kinases 6 (CDK6), thereby promoting apoptosis and arresting cells in the G1 phase 33,34. Previous studies showed that, when CDKN2B expression was upregulated, unbound Cyclin D was degraded by the ubiquitin-dependent proteasomal degradation pathway, causing cells to be arrested in the G1 phase 35,36.…”

Section: Discussionmentioning

confidence: 99%

<p>Cyclin-dependent kinase inhibitor 2B gene is associated with the sensitivity of hepatoma cells to Sorafenib</p>

Weng¹,

Zeng²,

Yan³

et al. 2019

OTT

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Purpose: The sensitivity of advanced hepatocellular carcinoma (HCC) to Sorafenib is low. The purpose of this study was to investigate the effects of cyclin-dependent kinase inhibitor 2B (CDKN2B) gene on the prognosis of HCC and the sensitivity of HCC cells to Sorafenib. Patients and methods: Streptavidin-perosidase (SP) staining was performed to determine the expression of CDKN2B in HCC tissues and adjacent tissues. The cell counting kit-8 (CCK-8) assay was carried out to determine cell viability. CDKN2B mRNA and protein were tested by real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot, respectively. CDKN2B gene was silenced or over-expressed in the cells by plasmid transfection technique. Flow cytometry was carried out to detect cell cycle and apoptosis. Results: SP staining results showed that CDKN2B was positive in adjacent tissues and in HCC tissues from partial response (PR) patients, CDKN2B was slightly positive in stable disease (SD) patients, but negative in progression disease (PD) patients. The survival rate of patients with low expression of CDKN2B was low. Up-regulation of CDKN2B expression could promote the pro-apoptotic effect of Sorafenib and cell arrest in G1 phase. When the CDKN2B gene expression was down-regulated, the cell apoptosis rate and the proportion of cells treated with Sorafenib in G1 phase decreased. Silencing CDKN2B reversed CDKN2B overexpression caused by Sorafenib. Conclusion: CDKN2B genes were lowly expressed in tumor tissues from HCC patients who were treated with Sorafenib and had a poor prognosis. Up-regulation of CDKN2B promoted sensitivity of HCC to Sorafenib, and similarly down-regulation of CDKN2B reduced the sensitivity.

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Section: Discussionmentioning

confidence: 99%

<p>Cyclin-dependent kinase inhibitor 2B gene is associated with the sensitivity of hepatoma cells to Sorafenib</p>

Weng¹,

Zeng²,

Yan³

et al. 2019

OTT

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“…Insight into the mechanisms by which ANRIL alters P15 INK4B and Bcl-2 expression was provided by a previous study that showed that ANRIL depletion could disrupt SUZ12, a component of the polycomb repressive complex 2 (PRC2), by binding to the P15 INK4B locus and increasing P15 INK4B expression [43]. Additionally, a recent study reported that P15 INK4B down-regulated Bcl-2 expression in chronic myeloid leukemia cells [44]. Collectively, our data and the previous findings suggest that P15 INK4B and Bcl-2 are key genes downstream of ANRIL that promote EOC cell proliferation.…”

Section: Discussionmentioning

confidence: 99%

The long non-coding RNA ANRIL promotes proliferation and cell cycle progression and inhibits apoptosis and senescence in epithelial ovarian cancer

et al. 2016

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Antisense non-coding RNA in the INK4 locus (ANRIL) has been implicated in a variety of cancers. In the present study, we evaluated ANRIL expression in epithelial ovarian cancer (EOC) and defined its clinical implications and biological functions. ANRIL was overexpressed in EOC tissues relative to normal controls. Overexpression correlated with advanced International Federation of Gynecologists and Obstetricians stage and high histological grade. Multivariate analysis indicated that ANRIL is an independent prognostic factor for overall survival in EOC. Gain- and loss-of-function experiments demonstrated that ANRIL promotes EOC cell proliferation both in vitro and in vivo. The proliferative effect was linked to the promotion of cell cycle progression and inhibition of apoptosis and senescence. Down-regulation of P15INK4B and up-regulation of Bcl-2 by ANRIL may partially explain ANRIL-induced EOC cell proliferation. This study is the first to establish that ANRIL promotes EOC progression and is a potential prognostic biomarker.

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“…CDKN2B (cyclin dependent protein kinase inhibitor 2B, or called p15 and INK4B) belongs to the INK4 protein family. Also known as multiple tumor suppressor (MTS1), it can inhibit the activity of cyclin-dependent kinase 4 (CDK4) or CDK6, which thereby inhibit cell cycle and cause G1 retardation of cells, thus inhibiting tumor cell proliferation and facilitating tumor cell apoptosis [ 13 , 14 ]. Some research has demonstrated that upregulating the expression of CDKN2B can promote the G1 retardation of HepG2/DDP, inhibit tumor cell proliferation, and enhance the accumulation and retention of chemotherapeutic drugs in cells [ 15 ].…”

Section: Discussionmentioning

confidence: 99%

CDKN2B is critical for verapamil-mediated reversal of doxorubicin resistance in hepatocellular carcinoma

Zhang

Huang

et al. 2017

Oncotarget

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In this study, we explored the function and mechanism of CDKN2B genes in verapamil (VER)-induced reversal of resistance to doxorubicin (ADM) chemotherapy in hepatocellular carcinoma (HCC). We examined 4 HCC cell lines and found that the expression levels of CDKN2B genes correlated with the level of apoptosis induced by ADM+VER. Overexpression of CDKN2B genes promoted apoptosis in cells treated with VER+ADM. CDKN2B knockdown using siRNA weakened the effect of ADM+VER, indicating that ADM+VER promotes HCC cell apoptosis and that CDKN2B genes participate in VER-mediated promotion in tumor cell apoptosis. Future research will further explore the functional mechanism, and the associated signal transduction pathways via which CDKN2B affects HCC drug resistance.

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A combination of STI571 and BCR-ABL1 siRNA with overexpressed p15INK4B induced enhanced proliferation inhibition and apoptosis in chronic myeloid leukemia

Cited by 6 publications

References 23 publications

<p>Cyclin-dependent kinase inhibitor 2B gene is associated with the sensitivity of hepatoma cells to Sorafenib</p>

<p>Cyclin-dependent kinase inhibitor 2B gene is associated with the sensitivity of hepatoma cells to Sorafenib</p>

The long non-coding RNA ANRIL promotes proliferation and cell cycle progression and inhibits apoptosis and senescence in epithelial ovarian cancer

CDKN2B is critical for verapamil-mediated reversal of doxorubicin resistance in hepatocellular carcinoma

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