High Sam68 expression predicts poor prognosis in non-small cell lung cancer

Zhang, Z.; Xu, Yiyue; Sun, Ning; Zhang, M.; Xie, Jian; Jiang, Zhongmin

doi:10.1007/s12094-014-1160-3

Cited by 17 publications

(17 citation statements)

References 24 publications

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“…It has been reported that high expression of Sam68 is a is a predictor of poor prognosis in non-small cell lung cancer, oral tongue cancer, early-stage cervical cancer and colorectal cancer (8,9,13,14). In the present study, the expression level of Sam68 was demonstrated to be higher in NB tissues compared with their matched adjacent normal tissues.…”

Section: Discussionsupporting

confidence: 54%

“…Previously, Sam68 was identified to be frequently upregulated in cancer and has an oncogenic role in inflammatory carcinogenesis, tumor invasion and metastasis (8,9). Sam68 is predicated to be a target gene of miR-203, according to bioinformatic analysis, however, whether miR-203 directly mediates the expression of Sam68 and their roles in NB remain to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA-203 inhibits the malignant progression of neuroblastoma by targeting Sam68

Zhao

Tian

et al. 2015

Molecular Medicine Reports

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Abstract. Neuroblastoma (NB) is the most common solid extracranial tumor in children. However, the molecular mechanism of NB remains to be elucidated. In the present study, reverse transcription quantitative polymerase chain reaction data demonstrated that the expression of Sam68 was significantly upregulated in NB tissues compared with their matched adjacent normal tissues. Furthermore, it was revealed that reduced expression of miR-203 and increased expression of Sam68 co-existed in NB tissues. Knockdown of Sam68 reduced the proliferation, migration and invasion of human SK-N-SH and SH-SY5Y NB cells. Similarly, overexpression of miR-203 also inhibited the proliferation, migration and invasion of these two cell lines. It was further demonstrated that the protein expression level of Sam68 was negatively mediated by miR-203 in the SK-N-SH and SH-SY5Y NB cells. Additionally, data from a dual luciferase reporter assay confirmed that miR-203 directly targeted Sam68 by binding to its 3'-untranslated region. In conclusion, the present study suggested for the first time, to the best of our knowledge, that the aberrant downregulation of miR-203 may contribute to the aberrant upregulation of Sam68 in NB and that miR-203 has an inhibitory role in malignant progression of NB by targeting Sam68. The present study provided evidence to support miR-203/Sam68 as a novel diagnostic or therapeutic targets for NB.

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Section: Discussionsupporting

confidence: 54%

Section: Introductionmentioning

confidence: 99%

MicroRNA-203 inhibits the malignant progression of neuroblastoma by targeting Sam68

Zhao

Tian

et al. 2015

Molecular Medicine Reports

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“…In agreement with the suggested oncogenic property, Sam68 has also been found to be overexpressed in breast cancer [17,20], prostate cancer [21,27], nonsmall cell lung cancer [24], and neuroblastoma [28]. These studies have suggested that Sam68 is upregulated in many malignant tumor, and its upregulation correlated with shorter survival rates.…”

Section: Discussionsupporting

confidence: 58%

“…Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) was used as an internal loading control. Experiments were performed in triplicate in three independent experiments.Western blotting was conducted according to the standard method as mentioned previously[24], using anti-Sam68 antibody (1:1000 dilution; Santa Cruz). Anti-α-tubulin antibody (1:1000 dilution; Santa Cruz) was used as the loading control.…”

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confidence: 99%

Clinical significance of Sam68 expression in endometrial carcinoma

Liu

Qin

et al. 2015

Tumor Biol.

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Sam68 (Src-associated in mitosis of 68 kDa) is a substrate for tyrosine kinase c-Src during mitosis. The nuclear protein level has been found to be associated with progression and prognosis in various human malignant tumors. The aim of this study is to investigate the clinical value of Sam68 in endometrial carcinoma (EC). Sam68 expression was confirmed by real-time PCR, Western blot, and immunofluorescent assay in primary normal endometrial epithelial cells, endometrial carcinoma cell lines, as well as seven pairs of EC and matched adjacent noncancerous endometrial tissues. Moreover, the protein level of Sam68 was evaluated by immunohistochemistry in a cohort of surgical specimens derived from 131 patients including primary endometrial carcinoma (n = 95), endometrial atypical hyperplasia (precancerous lesions, n = 26), and normal endometria (n = 10). In endometrial cancer cell lines, RNA interfering approach was employed to downregulate Sam68 expression to determine its role in proliferation. Clinicopathological relevance and prognostic associations were examined by statistical analyses. Compared with normal endometrial and endometrial atypical hyperplasia tissues, Sam68 significantly elevated in endometrial cancer samples (P < 0.01), which was negative or low in 37 cases (38.9 %) and high in 58 cases (61.1 %). The high expression of Sam68 was associated with histological grade (P < 0.001), FIGO stage (P = 0.039), and myometrial invasion (P = 0.002). Kaplan-Meier analysis demonstrated that overexpression of Sam68 correlated with shorter overall survival. It is confirmed by univariate and multivariate analysis (P < 0.001 and P = 0.048, respectively). Additionally, we found that Sam68 was highly expressed at both the transcriptional and translational levels in endometrial cancer cell lines (Ishikawa, HEC-1B, AN3CA, KLE, and RL95-2) and siRNA knockdown of Sam68 remarkably inhibited cellular proliferation in in vitro models. Sam68 may be useful prognostic marker for EC, and it plays an important role in promoting the cellular proliferation. Further investigation of Sam68 as a potential therapeutic target for EC patients could be of interest.

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“…The expression of Sam68 is often elevated in human cancers, including breast, colorectal, esophageal, endometrial, cervical, renal, lung, bladder, ovarian, neural, and prostate cancers [4–15]. Furthermore, overexpression of Sam68 has been shown to correlate with poor survival prognosis in renal cell carcinoma, colorectal cancer, and non-small cell lung cancer patients [5, 9, 10]. In some cancers, high expression of Sam68 correlates with low expression of certain miRNAs shown to target Sam68, such as in the case of miR-203 and miR-204 observed in neuroblastoma and breast cancer, respectively [13, 16].…”

Section: Introductionmentioning

confidence: 99%

The p53 status can influence the role of Sam68 in tumorigenesis

Ngo

Aleynikova

et al. 2016

Oncotarget

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The expression and activities of RNA binding proteins are frequently dysregulated in human cancer. Their roles, however, appears to be complex, with reports indicating both pro-tumorigenic and tumor suppressive functions. Here we show, using two classical mouse cancer models, that the role of KH-type RNA binding protein, Sam68, in tumor development can be influenced by the status of the p53 tumor suppressor. We demonstrate that in mice expressing wild type p53, Sam68-deficiency resulted in a higher incidence and malignancy of carcinogen-induced tumors, suggesting a tumor suppressive role for Sam68. In marked contrast, Sam68-haploinsufficiency significantly delayed the onset of tumors in mice lacking p53 and prolonged their survival, indicating that Sam68 accelerates the development of p53-deficient tumors. These findings provide considerable insight into a previously unknown relationship between Sam68 and the p53 tumor suppressor in tumorigenesis.

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High Sam68 expression predicts poor prognosis in non-small cell lung cancer

Abstract: Our results suggest that high Sam68 expression predicts poor prognosis of NSCLC patients, and Sam68 may be potentially a prognostic biomarker for NSCLC.

Cited by 17 publications

References 24 publications

MicroRNA-203 inhibits the malignant progression of neuroblastoma by targeting Sam68

MicroRNA-203 inhibits the malignant progression of neuroblastoma by targeting Sam68

Clinical significance of Sam68 expression in endometrial carcinoma

The p53 status can influence the role of Sam68 in tumorigenesis

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