RETRACTED ARTICLE: High expression level and nuclear localization of Sam68 are associated with progression and poor prognosis in colorectal cancer

Liao, Wen Ting; Liu, Jun Ling; Wang, Zheng Gen; Cui, Yan; Shi, Ling; Li, Ting Ting; Zhao, Xiao Hui; Chen, Xiu Ting; Ding, Yan; Song, Li

doi:10.1186/1471-230x-13-126

Cited by 25 publications

(20 citation statements)

References 38 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: 53%

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: 53%

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

Zhao

Tian

et al. 2015

Molecular Medicine Reports

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“…It was found that Sam68 could induce cervical cancer lymph node metastasis, which served as predictors of pelvic lymph node metastasis in cervical cancer patients [25]. In the colorectal cancer tissues, Sam68 was also elevated, and the high Sam68 expression level was significantly correlated with the characteristics of aggressive colorectal cancer [26]. The similar result was found in renal cell carcinoma [23].…”

Section: Discussionsupporting

confidence: 52%

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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“…Elevation in Sam68 protein levels has been proposed as a prognostic marker in multiple cancers (Chen et al, 2012; Liao et al, 2013; Song et al, 2010; Zhang et al, 2009), although the exact function of Sam68 in these cancers remains obscure. We recently revealed that Sam68 plays a crucial role in controlling DNA damage-induced PARP1 activation and PAR production; hence Sam68 deficiency dramatically dampens the PAR-dependent NF-κB signaling and DNA repair pathways initiated by DNA damage (Fu et al, 2016; Sun et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

Sam68/KHDRBS1-dependent NF-κB activation confers radioprotection to the colon epithelium in γ-irradiated mice

Sun

Wier

et al. 2016

eLife

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Previously we reported that Src-associated-substrate-during-mitosis-of-68kDa (Sam68/KHDRBS1) is pivotal for DNA damage-stimulated NF-κB transactivation of anti-apoptotic genes (Fu et al., 2016). Here we show that Sam68 is critical for genotoxic stress-induced NF-κB activation in the γ-irradiated colon and animal and that Sam68-dependent NF-κB activation provides radioprotection to colon epithelium in vivo. Sam68 deletion diminishes γ-irradiation-triggered PAR synthesis and NF-κB activation in colon epithelial cells (CECs), thus hampering the expression of anti-apoptotic molecules in situ and facilitating CECs to undergo apoptosis in mice post whole-body γ-irradiation (WBIR). Sam68 knockout mice suffer more severe damage in the colon and succumb more rapidly from acute radiotoxicity than the control mice following WBIR. Our results underscore the critical role of Sam68 in orchestrating genotoxic stress-initiated NF-κB activation signaling in the colon tissue and whole animal and reveal the pathophysiological relevance of Sam68-dependent NF-κB activation in colonic cell survival and recovery from extrinsic DNA damage.DOI: http://dx.doi.org/10.7554/eLife.21957.001

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RETRACTED ARTICLE: High expression level and nuclear localization of Sam68 are associated with progression and poor prognosis in colorectal cancer

Cited by 25 publications

References 38 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

Sam68/KHDRBS1-dependent NF-κB activation confers radioprotection to the colon epithelium in γ-irradiated mice

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