Abstract:IntroductionStomatin-like protein 2 (SLP-2), a member of the Stomatin superfamily, has been identified as an oncogenic-related protein and found to be up-regulated in multi-cancers. Nonetheless, the expression pattern and regulation of SLP-2 in human esophageal squamous cell carcinoma (ESCC) remain unexplored.MethodsImmunohistochemistry and immunofluorescence staining analysis were performed to show SLP-2 expression and location. RNAi method was used to inhibit specific protein expression. Transwell assay was … Show more
“…Furthermore, our data revealed expression of SLP-2 in the cytoplasm of PTC cells that was not associated with histological type, but significantly associated with tumor stage, which was confirmed by qPCR after analyzing 42 cases of PTC. The highest expression was found in stage T4 (tumor extension beyond the thyroid capsule) tumors, which is in agreement with a previous study that expression of SLP-2 is associated with invasiveness of ESCC (30). SLP-2 alterations occur early in the process of tumor formation, which may predispose to malignant transformation.…”
Papillary thyroid cancer (PTC) accounts for 80-90% of all cases of thyroid malignancies. Stomatin-like protein 2 (SLP-2) is a novel member of the stomatin superfamily and is found in several types of human tumors. However, whether it is expressed in human PTC is unknown. In the present study, we aimed to explore the diagnostic value of SLP-2 in patients with PTC and to investigate whether SLP-2 expression is regulated by transforming growth factor-β (TGF-β), a cytokine which plays an important role in PTC tumorigenesis. A total of 107 patients consisting of 99 cases of classical and 8 cases of follicular variant PTC was examined. The expression of SLP-2 mRNA and protein was examined by immunohistochemistry (IHC) and qPCR, respectively. We found that SLP-2 was overexpressed in human PTC. The expression of SLP-2 was significantly associated with clinicopathological features of the PTC cases. Particularly, increased SLP-2 expression was mainly correlated with primary tumors >1 cm in size, with late stage tumors and with metastatic lymph nodes. The expression of SLP-2 was correlated with the expression of Ki-67, a cell proliferation marker, in PTC tissues as detected by IHC. SLP-2 was upregulated by TGF-β1 in PTC cells as evaluated by western blotting. The present data revealed for the first time that patients with PTC exhibited SLP-2 overexpression that was associated with clinicopathological features. The correlation between SLP-2 expression and proliferation marker Ki-67 may be characteristic of PTC and may reflect PTC progression. SLP-2 was upregulated by TGF-β1, indicating a possible role of SLP-2 in PTC tumorigenesis. Our data suggest that SLP-2 may be considered as a useful diagnostic marker and therapeutic target for PTC.
“…Furthermore, our data revealed expression of SLP-2 in the cytoplasm of PTC cells that was not associated with histological type, but significantly associated with tumor stage, which was confirmed by qPCR after analyzing 42 cases of PTC. The highest expression was found in stage T4 (tumor extension beyond the thyroid capsule) tumors, which is in agreement with a previous study that expression of SLP-2 is associated with invasiveness of ESCC (30). SLP-2 alterations occur early in the process of tumor formation, which may predispose to malignant transformation.…”
Papillary thyroid cancer (PTC) accounts for 80-90% of all cases of thyroid malignancies. Stomatin-like protein 2 (SLP-2) is a novel member of the stomatin superfamily and is found in several types of human tumors. However, whether it is expressed in human PTC is unknown. In the present study, we aimed to explore the diagnostic value of SLP-2 in patients with PTC and to investigate whether SLP-2 expression is regulated by transforming growth factor-β (TGF-β), a cytokine which plays an important role in PTC tumorigenesis. A total of 107 patients consisting of 99 cases of classical and 8 cases of follicular variant PTC was examined. The expression of SLP-2 mRNA and protein was examined by immunohistochemistry (IHC) and qPCR, respectively. We found that SLP-2 was overexpressed in human PTC. The expression of SLP-2 was significantly associated with clinicopathological features of the PTC cases. Particularly, increased SLP-2 expression was mainly correlated with primary tumors >1 cm in size, with late stage tumors and with metastatic lymph nodes. The expression of SLP-2 was correlated with the expression of Ki-67, a cell proliferation marker, in PTC tissues as detected by IHC. SLP-2 was upregulated by TGF-β1 in PTC cells as evaluated by western blotting. The present data revealed for the first time that patients with PTC exhibited SLP-2 overexpression that was associated with clinicopathological features. The correlation between SLP-2 expression and proliferation marker Ki-67 may be characteristic of PTC and may reflect PTC progression. SLP-2 was upregulated by TGF-β1, indicating a possible role of SLP-2 in PTC tumorigenesis. Our data suggest that SLP-2 may be considered as a useful diagnostic marker and therapeutic target for PTC.
“…First, STOML2 might serve as a prognostic marker especially in human gallbladder cancer, gastric cancer, glioma, colorectal cancer, breast cancer, and pulmonary squamous cell carcinoma (19)(20)(21)(22)(23)(24). STOML2 is also involved in invasion, regulating cell growth and cell adhesion in human esophageal squamous cell carcinoma, glioma, and human endometrial adenocarcinoma (21,(25)(26)(27). In desmoid tumor that behaves aggressively by infiltrating tissues deeply, STOML2 overexpression is clinically related to PFS.…”
Purpose: Because desmoid tumors exhibit an unpredictable clinical course, translational research is crucial to identify the predictive factors of progression in addition to the clinical parameters. The main issue is to detect patients who are at a higher risk of progression. The aim of this work was to identify molecular markers that can predict progression-free survival (PFS).Experimental Design: Gene-expression screening was conducted on 115 available independent untreated primary desmoid tumors using cDNA microarray. We established a prognostic gene-expression signature composed of 36 genes. To test robustness, we randomly generated 1,000 36-gene signatures and compared their outcome association to our define 36-genes molecular signature and we calculated positive predictive value (PPV) and negative predictive value (NPV).Results: Multivariate analysis showed that our molecular signature had a significant impact on PFS while no clinical factor had any prognostic value. Among the 1,000 random signatures generated, 56.7% were significant and none was more significant than our 36-gene molecular signature. PPV and NPV were high (75.58% and 81.82%, respectively). Finally, the top two genes downregulated in no-recurrence were FECH and STOML2 and the top gene upregulated in no-recurrence was TRIP6.Conclusions: By analyzing expression profiles, we have identified a gene-expression signature that is able to predict PFS. This tool may be useful for prospective clinical studies.
“…Reports have indicated that STOML-2 was upregulated in several kinds of tumor tissue and was involved in invasion and metastasis of cancers including esophageal cancer, gastric cancer, breast cancer and glioma (19)(20)(21)(22)(23). Inhibition of STOML-2 was able to decrease cell growth and proliferation, and reduced migratory speed and invasive ability (24,25).…”
Newly discovered intrinsic regulators, the miRNAs regulate gene expression by binding to the 3'-untranslated regions of the genome. Accumulating studies have indicated that miRNAs are aberrantly expressed in various human cancers. We found that miRNA-1207-5p (miR‑1207-5p) was markedly downregulated in esophageal carcinoma (EC) tissues, and was correlated with EC differentiation, pathological stage and lymph node metastasis. Rates of apoptosis were increased and cell invasion ability was decreased in EC9706 and EC-1 cells transfected with a miR‑1207-5p mimic. Stomatin-like protein 2 (STOML-2) was predicted to be a potential target of miR‑1207-5p by bioinformatics analysis and this was confirmed by luciferase assay and western blotting. Our study showed that STOML-2 was negatively regulated by miR‑1207-5p. Furthermore, overexpression of STOML-2 abolished the miR‑1207-5p anti-invasion function. Based on these results, we proposed that miR‑1207-5p might act as a potential therapeutic target in the treatment of EC.
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