Modulation of apoptosis by the cyclin-dependent kinase inhibitor p27Kip1

Hiromura, Keiju; Pippin, Jeffrey W.; Fero, Matthew L.; Roberts, James M.; Shankland, Stuart J.

doi:10.1172/jci5461

Cited by 206 publications

(164 citation statements)

References 41 publications

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“…The fact that cell cycle inhibitors could override the inhibitory e ects of DN-STAT3 mutants on G-CSF-induced di erentiation argues in that direction. However, it has recently been suggested that p27 might exert additional functions, such as prevention of apoptosis in mesangial cells and ®broblasts (Hiromura et al, 1999). The data presented here and elsewhere Ward et al, 199b) linking activation of STAT3 to both di erentiation and cell survival suggest that p27 has a similar survival promoting activity in di erentiating myeloid cells.…”

Section: Discussionsupporting

confidence: 58%

STAT3-mediated differentiation and survival of myeloid cells in response to granulocyte colony-stimulating factor: role for the cyclin-dependent kinase inhibitor p27Kip1

et al. 2000

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Section: Discussionsupporting

confidence: 58%

STAT3-mediated differentiation and survival of myeloid cells in response to granulocyte colony-stimulating factor: role for the cyclin-dependent kinase inhibitor p27Kip1

et al. 2000

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“…Some groups demonstrate the induction of growth arrest by p27 KIPl (Sherr and Roberts, 1995;Craig et al, 1997). Others show that p27 KIP1 expression induces apoptosis in several cell lines Schreiber et al, 1999), while p27 KIPl protects cells from apoptosis (Hiromura et al, 1999). In the present study, p27 KIP1 induced autophagic cell death, but not apoptosis in malignant glioma cells.…”

Section: Discussionsupporting

confidence: 48%

Antitumour effect of cyclin-dependent kinase inhibitors (p16INK4A, p18INK4C, p19INK4D, p21WAF1/CIP1 and p27KIP1) on malignant glioma cells

et al. 2003

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Cyclin-dependent kinase inhibitors (CDKIs) are considered as novel anticancer agents because of their ability to induce growth arrest or apoptosis in tumour cells. It has not yet been fully determined, however, which CDKI is the best candidate for the treatment of malignant gliomas and whether normal brain tissues are affected by CDKI expression. Using recombinant adenoviral vectors that express CDKIs (p16 INK4A , p18 INK4C , p19 INK4D , p21 WAF1/CIP1 and p27 KIP1 ), we compared the antitumour effect of CDKIs on malignant glioma cell lines (A172, GB-1, T98G, U87-MG, U251-MG and U373-MG). p27 KIP1 showed higher ability to suppress the growth of all tumour cells tested than other CDKIs. Interestingly, overexpression of p27 KIP1 induced autophagic cell death, but not apoptosis in tumour cells. On the other hand, p27 KIP1 overexpression did not inhibit the viability of cultured astrocytes (RNB) nor induced autophagy. Overall, our findings suggest that gene transfer of p27 KIP1 may be a promising approach for the therapy of malignant gliomas.

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“…In prostate cancer, p27 expression progressively declines with increasing tumour grade and stage [14,15]. p27 protein has also been shown to have a critical role in promoting apoptosis in breast, renal, lung and prostate cancer cell lines [5,[16][17][18][19]. Our findings are therefore in close agreement with those of Katner et al [5], who found that p27 significantly reduced the proliferation of prostate cancer cell lines, causing a visible increase in cellular apoptosis and accumulation of cells at G 0 /G 1 .…”

Section: Discussionmentioning

confidence: 99%

Exogenous p27KIP1 expression induces anti-tumour effects and inhibits the EGFR/PI3K/Akt signalling pathway in PC3 cells

Xia¹,

Luo²,

Wang³

2009

Asian J Androl

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Abstractp27 is a cyclin-dependent kinase inhibitor that regulates the progression of cells from G 1 to S phase of the cell cycle. Loss of p27 has been associated with disease progression and with an unfavourable outcome in prostate cancer. In this study, we investigated whether exogenous p27 expression in the human androgen-independent prostate cancer PC3 cell line had any effect on cell growth, and we studied the molecular mechanisms involved. p27 expression was restored in PC3 cells by plasmid delivery. Cell proliferation and apoptosis were assessed in PC3 cells transfected with p27. We also investigated the effects of p27 on the epidermal growth factor receptor (EGFR)/ phosphatidylinositol 3-kinase (PI3K)/Akt signalling pathway in PC3 cells. By restoring p27 expression in PC3 cells, we observed that p27 reduced proliferation and induced arrest in G 0 /G 1 phase. Moreover, p27-transfected PC3 cells underwent apoptosis, as shown by flow cytometric analysis and western blotting analysis of Bcl-2, Bax, Bad, caspase-3 and poly(ADP-ribose)polymerase expression. Furthermore, the p27-induced anti-tumour action correlated with inhibition of the EGFR/PI3K/Akt signalling pathway, as confirmed by western blotting analysis and densitometry of EGFR, PI3K (p85), Akt and p-Akt S473 expression. Our results suggest that exogenous expression of p27 inhibits the proliferation of PC3 cells through induction of G 1 arrest and apoptosis, and this process correlates with inhibition of the EGFR/PI3K/Akt signalling pathway.

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Modulation of apoptosis by the cyclin-dependent kinase inhibitor p27Kip1

Cited by 206 publications

References 41 publications

STAT3-mediated differentiation and survival of myeloid cells in response to granulocyte colony-stimulating factor: role for the cyclin-dependent kinase inhibitor p27Kip1

STAT3-mediated differentiation and survival of myeloid cells in response to granulocyte colony-stimulating factor: role for the cyclin-dependent kinase inhibitor p27Kip1

Antitumour effect of cyclin-dependent kinase inhibitors (p16INK4A, p18INK4C, p19INK4D, p21WAF1/CIP1 and p27KIP1) on malignant glioma cells

Exogenous p27KIP1 expression induces anti-tumour effects and inhibits the EGFR/PI3K/Akt signalling pathway in PC3 cells

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