Differential expression and role of p21cip/waf1 and p27kip1 in TNF-α-induced inhibition of proliferation in human glioma cells

Kumar, Pabbisetty Sudheer; Shiras, Anjali; Das, Gowry; Jagtap, Jayashree C.; Prasad, Vandna; Shastry, Padma

doi:10.1186/1476-4598-6-42

Cited by 20 publications

(17 citation statements)

References 56 publications

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“…12 Overexpression of p21 but not p27 prevents proliferation of human glioma cells. 31 These results indicate that p21 may be a major regulator of p53-induced cell growth arrest in VSMCs, as well as in certain cancer cells. The observations gleaned from the present study indicate that the upregulation of p21 mediated by activated p53 results in the suppression of cyclin E and cyclin D (Figure 2D), which leads to the inhibition of the formation of cyclin D/E and cyclin-dependent kinase (CDK) complexes.…”

Section: Discussionmentioning

confidence: 82%

Activation of NAD(P)H:Quinone Oxidoreductase 1 Prevents Arterial Restenosis by Suppressing Vascular Smooth Muscle Cell Proliferation

Kim

Jeoung²,

Oh³

et al. 2009

Circulation Research

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Section: Discussionmentioning

confidence: 82%

Activation of NAD(P)H:Quinone Oxidoreductase 1 Prevents Arterial Restenosis by Suppressing Vascular Smooth Muscle Cell Proliferation

Kim

Jeoung²,

Oh³

et al. 2009

Circulation Research

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“…The role of TNF-α is controversial; some investigations have proved apoptotic or necrotic effects of TNF-α, while others furnished evidence that endogenous TNF-α activates cellular growth and tumor progression [19]. …”

Section: Resultsmentioning

confidence: 99%

TNF-α Gene Knockout in Triple Negative Breast Cancer Cell Line Induces Apoptosis

Pileczki

Braicu

Gherman

et al. 2012

IJMS

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Tumor necrosis factor alpha (TNF-α) is a pro-inflammatory cytokine involved in the promotion and progression of cancer, including triple negative breast cancer cells. Thus, there is significant interest in understanding the molecular signaling pathways that connect TNF-α with the survival of tumor cells. In our experiments, we used as an in vitro model for triple negative breast cancer the cell line Hs578T. The purpose of this study is to determine the gene expression profiling of apoptotic signaling networks after blocking TNF-α formation by using specially designed siRNA molecules to target TNF-α messenger RNA. Knockdown of TNF-α gene was associated with cell proliferation inhibition and apoptosis, as observed by monitoring the cell index using the xCELLigence RTCA System and flow cytometry. PCR array technology was used to examine the transcript levels of 84 genes involved in apoptosis. 15 genes were found to be relevant after comparing the treated group with the untreated one of which 3 were down-regulated and 12 up-regulated. The down-regulated genes are all involved in cell survival, whereas the up-regulated ones are involved in and interact with pro-apoptotic pathways. The results described here indicate that the direct target of TNF-α in the Hs578T breast cancer cell line increases the level of certain pro-apoptotic factors that modulate different cellular networks that direct the cells towards death.

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“…35 We in our earlier studies showed that p21 functions as an inhibitor of cell proliferation in LN-18 glioma cells. 36 It is demonstrated that various transformation events induce downregula- tion of p21, followed by activation of AKT or ERK2, which interacts and phosphorylates p21, thereby promoting p21Cip1 nucleo-cytoplasmic translocation and ubiquitin-dependent degradation, resulting in cell cycle progression. 37 Several studies suggest that localization of p21 (Cip1) to the cytoplasm in transformed cells contributes to pathways that favor not only cell proliferation but also cell motility, thereby contributing to invasion and metastasis.…”

Section: Discussionmentioning

confidence: 99%

Dlxin-1, a member of MAGE family, inhibits cell proliferation, invasion and tumorigenicity of glioma stem cells

et al. 2010

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We have previously reported the presence of Dlxin-1, a member of the melanoma antigen gene (MAGE) family, in the brain and showed its function as a cell cycle arrest protein, suggesting that Dlxin-1 may have anti-proliferative functions in rapidly growing tumors. Using the cancer stem cell hypothesis, which attributes the initiation and progression of brain tumors to the cancerinitiating stem cells, we have investigated the role of Dlxin-1 in the glioma stem cells propagated by us as a cell culture system comprising of HNGC-2 cells. Our studies provide evidence about the role of Dlxin-1 as an anti-tumorigenic protein in the highly chemo-resistant glioma stem cells. Next, we show that these anti-proliferative effects are manifested by Dlxin-1 through down regulation of the activities of MMP-2 and MMP-9, and through interaction of Dlxin-1 with its target protein P311 that is involved in glioma cell invasion. In summary, we establish the roles for Dlxin-1, one as an anti-tumorigenic and anti-invasive protein in highgrade gliomas and the other as an inducer of differentiation of glioma stem cells. These two attributes, in conjunction, result in conversion of the drug-resistant brain tumor stem cells to the tumor-attenuated cells that may now be more amenable to effective therapeutic targeting.

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Differential expression and role of p21cip/waf1 and p27kip1 in TNF-α-induced inhibition of proliferation in human glioma cells

Cited by 20 publications

References 56 publications

Activation of NAD(P)H:Quinone Oxidoreductase 1 Prevents Arterial Restenosis by Suppressing Vascular Smooth Muscle Cell Proliferation

Activation of NAD(P)H:Quinone Oxidoreductase 1 Prevents Arterial Restenosis by Suppressing Vascular Smooth Muscle Cell Proliferation

TNF-α Gene Knockout in Triple Negative Breast Cancer Cell Line Induces Apoptosis

Dlxin-1, a member of MAGE family, inhibits cell proliferation, invasion and tumorigenicity of glioma stem cells

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