Elevated expression of protein regulator of cytokinesis 1, involved in the growth of breast cancer cells

Shimo, Arata; Nishidate, Toshihiko; Ohta, Tomohiko; Fukuda, Mamoru; Nakamura, Yusuke; Katagiri, Toyomasa

doi:10.1111/j.1349-7006.2006.00381.x

Cited by 95 publications

(97 citation statements)

References 30 publications

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“…PRC1 also referred to as protein regulator of cytokinesis 1, contains two Cdk phosphorylation motifs, and phosphorylation is possibly important to mitotic suppression of bundling (24), which overexpression extensively bundles interphase microtubules (24). PRC1 also involved in the formation of cancer, research shows that the expression of PRC1 is upregulated in the development of breast cancer (25). Similar to KIFC1, endogenous PRC1 levels was significant increase in G2/M phase using breast cancer cell lines (25), and KIF14 targets to the central spindle via its interaction with PRC1 and has an essential function in cytokinesis (26).…”

Section: Discussionmentioning

confidence: 99%

The overexpression of KIFC1 was associated with the proliferation and prognosis of non-small cell lung cancer

Liu¹,

Zhan²,

Zhou³

et al. 2016

J. Thorac. Dis.

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Background: The kinesin family member C1 (KIFC1, also known as HSET) is a kinesin superfamily protein (KIFs). Although KIFC1 acts as a crucial role in the development of several human cancers, the KIFC1 expression profile and functional remain unclear in non-small cell lung cancer (NSCLC). Methods:We collected the fresh NSCLC samples and paired normal lung tissue in patients with lung cancer operation, and detected KIFC1 expression using quantitative reverse-transcription polymerase chain reaction (qRT-PCR) and Western blotting. To expand on previous smaller-scale studies, NSCLC tissue microarrays (TMA) were analyzed by IHC. Finally, cell lines were employed to further probe the potential mechanisms, Results:In this study, we described that KIFC1 was significantly upregulated in NSCLC tissues compared with the corresponding normal tissues. Moreover, KIFC1 overexpression was associated with the poor overall survival (OS) of NSCLC patients, and siRNA-mediated knockdown of KIFC1 significantly suppressed tumor cell proliferation in vitro. Further verification showed that inhibition of KIFC1 gene expression caused the upregulation of the cyclin-dependent kinases inhibitor p21 and downregulation of the cell cycle driver protein cdc2, which arrested cells in the G2-M phase.Conclusions: we report that increased KIFC1 expression may promote cell proliferation and identified it as a biomarker of unfavorable prognosis in NSCLC patients.Keywords: Kinesin family member C1 (KIFC1); non-small cell lung cancer (NSCLC); cyclin-dependent kinase inhibitor 1A (p21); cell division cycle protein 2 homolog (cdc2); prognostic

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Section: Discussionmentioning

confidence: 99%

The overexpression of KIFC1 was associated with the proliferation and prognosis of non-small cell lung cancer

Liu¹,

Zhan²,

Zhou³

et al. 2016

J. Thorac. Dis.

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“…010005T, MA05-317T, 010069T and 010571T), normal mammary tissue (sample no. 10441N), breast cancer tissuearrays (COSMOBIO, Tokyo, Japan) and other normal human tissues (lung, heart, liver, kidney, colon, pancreas, skeletal muscle, small intestine and testis; Biochain, Hayward, CA, USA) were processed for antigen retrieval by autoclave in accordance with the previous report (Shimo et al, 2007). Tissue sections were incubated with anti-DTL/RAMP polyclonal antibody as primary antibody at 1:50 followed by horseradish peroxidase-cojugated secondary antibody (DakoCytomation, Carpinteria, CA, USA).…”

Section: Western Blot Analysismentioning

confidence: 99%

“…Through the genome-wide expression analysis we have isolated a number of genes that function as oncogenes in the process of development and/or progression of breast cancers (Park et al, 2006;Lin et al, 2007;Shimo et al, 2007), synovial sarcomas (Nagayama et al, 2004(Nagayama et al, , 2005 and renal cell carcinomas (Togashi et al, 2005;Hirota et al, 2006). Such molecules are considered to be candidate targets for development of new therapeutic modalities.…”

Section: Introductionmentioning

confidence: 99%

Involvement of elevated expression of multiple cell-cycle regulator, DTL/RAMP (denticleless/RA-regulated nuclear matrix associated protein), in the growth of breast cancer cells

et al. 2008

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To investigate the detailed molecular mechanism of mammary carcinogenesis and discover novel therapeutic targets, we previously analysed gene expression profiles of breast cancers. We here report characterization of a significant role of DTL/RAMP (denticleless/RA-regulated nuclear matrix associated protein) in mammary carcinogenesis. Semiquantitative RT-PCR and northern blot analyses confirmed upregulation of DTL/RAMP in the majority of breast cancer cases and all of breast cancer cell lines examined. Immunocytochemical and western blot analyses using anti-DTL/RAMP polyclonal antibody revealed cell-cycle-dependent localization of endogenous DTL/RAMP protein in breast cancer cells; nuclear localization was observed in cells at interphase and the protein was concentrated at the contractile ring in cytokinesis process. The expression level of DTL/RAMP protein became highest at G 1 /S phases, whereas its phosphorylation level was enhanced during mitotic phase. Treatment of breast cancer cells, T47D and HBC4, with small-interfering RNAs against DTL/RAMP effectively suppressed its expression and caused accumulation of G 2 /M cells, resulting in growth inhibition of cancer cells. We further demonstrate the in vitro phosphorylation of DTL/ RAMP through an interaction with the mitotic kinase, Aurora kinase-B (AURKB). Interestingly, depletion of AURKB expression with siRNA in breast cancer cells reduced the phosphorylation of DTL/RAMP and decreased the stability of DTL/RAMP protein. These findings imply important roles of DTL/RAMP in growth of breast cancer cells and suggest that DTL/RAMP might be a promising molecular target for treatment of breast cancer.

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“…Through the genome-wide expression analysis, we have isolated a number of genes that functioned as oncogenes in the process of development and/or progression of breast cancers (Park et al, 2006;Shimo et al, 2007), hepatocellular carcinomas (Hamamoto et al, 2004), pancreatic cancer (Taniuchi et al, 2005a, b), prostate cancers Ashida et al, 2005), synovial sarcomas (Nagayama et al, 2004(Nagayama et al, , 2005 and renal cell carcinomas (Togashi et al, 2005). Such molecules are considered to be good candidate targets for development of new therapeutic modalities.…”

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confidence: 99%

Involvement of upregulation of DEPDC1 (DEP domain containing 1) in bladder carcinogenesis

et al. 2007

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In an attempt to disclose mechanisms of bladder carcinogenesis and discover novel target molecules for development of treatment, we applied a cDNA microarray to screen genes that were significantly transactivated in bladder cancer cells. Among the upregulated genes, we here focused on a novel gene, (DEPDC1) DEP domain containing 1, whose overexpression was confirmed by northern blot and immunohistochemical analyses. Immunocytochemical staining analysis detected strong staining of endogenous DEPDC1 protein in the nucleus of bladder cancer cells. Since DEPDC1 expression was hardly detectable in any of 24 normal human tissues we examined except the testis, we considered this gene-product to be a novel cancer/testis antigen. Suppression of DEPDC1 expression with small-interfering RNA significantly inhibited growth of bladder cancer cells. Taken together, these findings suggest that DEPDC1 might play an essential role in the growth of bladder cancer cells, and would be a promising molecular-target for novel therapeutic drugs or cancer peptide-vaccine to bladder cancers.

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Elevated expression of protein regulator of cytokinesis 1, involved in the growth of breast cancer cells

Cited by 95 publications

References 30 publications

The overexpression of KIFC1 was associated with the proliferation and prognosis of non-small cell lung cancer

The overexpression of KIFC1 was associated with the proliferation and prognosis of non-small cell lung cancer

Involvement of elevated expression of multiple cell-cycle regulator, DTL/RAMP (denticleless/RA-regulated nuclear matrix associated protein), in the growth of breast cancer cells

Involvement of upregulation of DEPDC1 (DEP domain containing 1) in bladder carcinogenesis

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