SIRT1 Expression Is Associated with Good Prognosis in Colorectal Cancer

Jung, Wonkyung; Hong, Kwang Dae; Jung, Woon Yong; Lee, Eunjung; Shin, Bong Kyung; Kim, Han Kyeom; Kim, Aeree; Kim, Baek Hui

doi:10.4132/koreanjpathol.2013.47.4.332

Cited by 44 publications

(38 citation statements)

References 25 publications

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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.…”

Section: A B C Dsupporting

confidence: 80%

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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Section: A B C Dsupporting

confidence: 80%

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

Lin¹,

Peng²

2015

Oncology Letters

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“…Presently, several paper reported that the relationship Xiu-Lai Zhang, Min-Li Chen, Sheng-Li Zhou* between Sirt1 and colorectal cancer involved in tumor malignant degree, transfer, patient survival rate and cancer cell proliferation (Kabra et al, 2009;Jung et al, 2013;Lv et al, 2014). Whether sirt1 acting as a cancer-promoting genes or a tumor suppressor gene is always a controversy.…”

Section: Introductionmentioning

confidence: 99%

Fentanyl Increases Colorectal Carcinoma Cell Apoptosis by Inhibition of NF-κB in a Sirt1-dependent Manner

Zhang¹,

Chen²,

Zhou³

2014

Asian Pacific Journal of Cancer Prevention

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Background: Fentanyl is used as an analgesic to treat pain in a variety of patients with cancer and recently it has become considered to also act as an antitumor agent. The study present was designed to investigate the effects of fentanyl on colorectal cancer cell growth and plausible mechanisms. Materials and Methods: The human colorectal carcinoma cell line HCT116 was subcutaneously injected into nude mice. The viability of HCT116 was tested by MTT assay, and apoptosis by flow cytometry and caspase-3 activity. The expression of Sirt1 and NF-κB were evaluated by Western blotting and the levels of Sirt1 and NF-κB by fluorescence method. SiRNA was used to silence and Ad-Sirt1 to overexpress Sirt1. Results: Our data showed that fentanyl could inhibit tumor growth, with increased expression of Sirt1 and down-regulation of Ac-p65 in tumors. Compared with control cells without treatment, HCT116 cells that were incubated with fentanyl had a higher apoptotic rate. Moreover, fentanyl could increase expression and activity of Sirt1 and inhibitor expression and activity of NF-κB, which might be mechanisms of fentanyl action. Conclusions: Fentanyl increased colorectal carcinoma cell apoptosis by inhibition of NF-κB activation in a Sirt1-dependent manner.

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“…In contrast, in several other cancer types, including breast, liver, and gastric cancers, overexpression of SIRT1 is associated with poor prognosis, implying a role for SIRT1 in cancer promotion [13][14][15][16]. In colon cancer, the implications of high expression levels of SIRT1 remain controversial [17][18][19][20][21]. Consistent with these in vivo observations, in vitro studies have shown context-dependent roles of SIRT1 in cancer cells [22][23][24].…”

Section: Introductionmentioning

confidence: 76%

Association of SIRT1 and tumor suppressor gene TAp63 expression in head and neck squamous cell carcinoma

et al. 2015

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Expression of the protein deacetylase SIRT1 is associated with either poor or favorable prognosis in cancer patients, depending on the cancer type. In head and neck squamous cell carcinoma (HNSCC), SIRT1 expression is associated with favorable prognosis. However, the molecular mechanism underlying the tumor-suppressive function of SIRT1 in HNSCC is unknown. SIRT1 promotes differentiation in epithelial cells; therefore, we investigated whether SIRT1 promotes differentiation in HNSCC cells by studying the correlations between the expression of SIRT1 and several genes implicated in stemness or differentiation in HNSCC-derived cell lines. Our results suggest that SIRT1 does not contribute to differentiation in HNSCC cells. RNA interference-mediated reduction of SIRT1 revealed that SIRT1 supports the expression of TAp63, which has been implicated in tumor suppression, in addition to epithelial differentiation. A positive correlation was observed between SIRT1 and TAp63 expression in HNSCC tissues, as determined by quantitative reverse transcription-polymerase chain reaction analysis of RNA extracted from formalin-fixed paraffin-embedded biopsy samples. Together, these results suggest that although SIRT1 does not regulate differentiation of HNSCC cells, it functions as a tumor suppressor in HNSCC by supporting the transcription of tumor-suppressive TAp63. This finding supports the notion that SIRT1-activating drugs could be useful for the treatment of HNSCC.

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SIRT1 Expression Is Associated with Good Prognosis in Colorectal Cancer

Cited by 44 publications

References 25 publications

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

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

Fentanyl Increases Colorectal Carcinoma Cell Apoptosis by Inhibition of NF-κB in a Sirt1-dependent Manner

Association of SIRT1 and tumor suppressor gene TAp63 expression in head and neck squamous cell carcinoma

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