Expression and prognostic significance of SIRT1 in ovarian epithelial tumours

Jang, Kyu Yun; Kim, Kwan Sik; Hwang, Sung Ho; Kwon, Keun Sang; Kim, Kyung Ryoul; Park, Ho Sung; Park, Byung‐Hyun; Chung, Myoung Ja; Kang, Myoung Jae; Lee, Dong Geun; Moon, Woo Sung

doi:10.1080/00313020902884451

Cited by 112 publications

(104 citation statements)

References 20 publications

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“…In contrast to our results, a previous study demonstrated the down-regulation of sIrt1 in colon tumors (23) and its antitumor properties (24). Despite frequent overexpression of sIrt1 in malignant ovarian serous tumors, increased expression of sIrt1 showed a correlation with increased overall survival (15). In addition, a recent study demonstrated suppressed intestinal tumor formation due to enhanced sIrt1 expression in a β-catenindependent mouse model of colon cancer, thereby indicating that the effects of sIrt1 may vary in different tumor models, depending on downstream targets of the enzyme (25).…”

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confidence: 99%

“…Up-regulation of sIrt1 induces deacetylated inactivation of p53, which allows proliferation of cells in the presence of damaged DNA such that mutations accumulate, including those in p53 itself, leading to disruption of the cell cycle control and promotion of tumor progression (6)(7)(8)(9)(10)(11). recent studies have demonstrated overexpression of sIrt1 in cancer tissue, compared with normal tissue, suggesting that sIrt1 may act as a tumor promoter (9,(12)(13)(14)(15)(16). However, expression of sIrt1 in HCC and its role have not been investigated.…”

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Expression and role of SIRT1 in hepatocellular carcinoma

Choi

Bae²,

Jamiyandorj³

et al. 2011

Oncol Rep

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Abstract. silent mating type information regulation 2 homolog 1 (sIrt1) is a multifaceted, nicotinamide adenine dinucleotide-dependent protein deacetylase with involvement in a wide variety of cellular processes ranging from cancer to aging. expression of sIrt1 was evaluated in 90 cases of hepatocellular carcinoma (HCC) and five HCC cell lines. The relationship between the mutation status of p53 and expression of sIrt1 was also investigated in 10 fresh HCC tissues. synthetic small interfering rNA was used to silence sIrt1 gene expression by rNA interference (rNAi), and cell growth and cell cycle progression were assessed. expression of sIrt1 was significantly elevated in the HCC tissues when compared to that of non-tumor tissues (p<0.001). Overexpression of sIrt1 and p53 was observed in 56% (50 of 90) and in 30% (27 of 90) of the HCCs, respectively. expression of sIrt1 showed significant correlation with gender (p=0.023), serum AFP levels (p=0.030), viral infection (p=0.005) and p53 expression (p<0.021). Western blot analysis found no correlation between p53 mutation and expression levels of sIrt1. sIrt1 silencing was found to induce cell growth arrest in HCC cells. these results suggest an association of sIrt1 expression with HCC development and that sIrt1 plays a role in cancer cell growth.

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confidence: 99%

Expression and role of SIRT1 in hepatocellular carcinoma

Choi

Bae²,

Jamiyandorj³

et al. 2011

Oncol Rep

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“…The present study identified an association of SIRT1 overexpression with shorter OS time and poor prognostic indicators in SCC, which was consistent with the results of previous studies (4,36,45). By contrast, certain reports have found a significant association between SIRT1 overexpression and more favorable prognosis in serous carcinoma of the ovary (46) and colorectal cancer (47,48). In the present study, Kaplan-Meier survival analysis suggested that patients with tumor invasion (P=0.043), lymph node metastasis (P<0.001), larger tumor size (P=0.047) and higher pathological T stage (P=0.001) have poorer prognoses (Fig.…”

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confidence: 93%

Association of SIRT1 and HMGA1 expression in non-small cell lung cancer

Lin¹,

Peng²

2015

Oncology Letters

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Abstract. The roles of Silent mating type information regulation 2 homolog 1 (SIRT1) and High mobility group A1 (HMGA1) in human diseases have been extensively studied separately; however, to the best of our knowledge, the current study is the first to report on their interrelationship in lung cancer. The association of SIRT1 and HMGA1 in non-small cell lung cancer (NSCLC) was investigated by evaluating their expression and prognostic significance in 260 patients with NSCLC using immunohistochemistry. SIRT1 and HMGA1 expression were found to be significantly correlated with each other (P<0.001), and both were significantly associated with clinicopathological parameters, including histological type and degree of differentiation. In squamous cell carcinoma (SCC), SIRT1 + specimens were significantly associated with shorter overall survival (OS) time (P=0.019). However, in patients with adenocarcinoma (AD), no association was identified between SIRT1 and OS. In addition, HMGA1 + specimens were significantly associated with poor differentiation (P=0.028), and were more frequent in SCC than AD (P=0.015). However, HMGA1 was not associated with OS on univariate Cox regression analysis or Kaplan-Meier analysis (both P>0.05). SIRT1/HMGA1 coexpression was significantly associated with male gender (P=0.016), and moderately and poorly differentiated histological grade (P=0.025). The findings indicate that SIRT1 and HMGA1 may have significant effects during tumor progression in NSCLC, particularly in patients with SCC, and are potentially useful as prognostic indicators for patients with NSCLC.

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“…SIRT1 is overexpressed in multiple primary solid tumors and hematopoietic malignancies (Bradbury et al, 2005;Huffman et al, 2007;Jang et al, 2008Jang et al, , 2009Jung-Hynes et al, 2009;Nosho et al, 2009). Inhibition of SIRT1 suppresses growth and promotes apoptosis in human cancer cells (Luo et al, 2001;Vaziri et al, 2001;Chu et al, 2005;Ford et al, 2005;Ota et al, 2006;Kojima et al, 2008;Jung-Hynes et al, 2009), but has little impact on the survival of normal cells (Ford et al, 2005;Jung-Hynes et al, 2009).…”

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confidence: 99%

NAMPT overexpression in prostate cancer and its contribution to tumor cell survival and stress response

et al. 2010

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Nicotinamide phosphoribosyltransferase (NAMPT) is a rate-limiting enzyme in regenerating nicotinamide adenine dinucleotide (NAD þ ) from nicotinamide in mammals. NAMPT has crucial roles for many cellular functions by regulating NAD þ -dependent SIRT1 deacetylase. However, roles of NAMPT in cancer are poorly defined. In this study, we show that NAMPT is prominently overexpressed in human prostate cancer cells along with SIRT1. Elevation of NAMPT expression occurs early for the prostate neoplasia. Inhibition of NAMPT significantly suppresses cell growth in culture, soft agar colony formation, cell invasion and growth of xenografted prostate cancer cells in mice. NAMPT knockdown sensitizes prostate cancer cells to oxidative stress caused by H 2 O 2 or chemotherapeutic treatment. Overexpression of NAMPT increases prostate cancer cell resistance to oxidative stress, which is partially blocked by SIRT1 knockdown. We demonstrate that in addition to modulating SIRT1 functions, the NAMPT inhibition reduces forkhead box, class 'O' (FOXO)3a protein expression and its downstream anti-oxidant genes catalase and manganese superoxide dismutase. Our results suggest important roles of concomitant upregulation of NAMPT and SIRT1 along with increased FOXO3a protein level for prostate carcinogenesis and their contribution to oxidative stress resistance of prostate cancer cells. These findings may have implications for exploring the NAMPT pathway for prostate cancer prevention and treatment.

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Expression and prognostic significance of SIRT1 in ovarian epithelial tumours

Cited by 112 publications

References 20 publications

Expression and role of SIRT1 in hepatocellular carcinoma

Expression and role of SIRT1 in hepatocellular carcinoma

Association of SIRT1 and HMGA1 expression in non-small cell lung cancer

NAMPT overexpression in prostate cancer and its contribution to tumor cell survival and stress response

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