Suppression of scinderin modulates epithelial-mesenchymal transition markers in highly metastatic gastric cancer cell line SGC-7901

Chen, Xiaomin; Guo, Junming; Chen, Ping; Mao, Liangang; Wei-yun, Feng; Donghai, Le; Li, Keqiang

doi:10.3892/mmr.2014.2523

Cited by 17 publications

(14 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In agreement with our report, SCIN expression levels were shown to correlate with poor overall survival in patients with gastric cancers, and silencing of SCIN effectively suppressed the migratory and invasive capabilities and tumourigenicity . SCIN knockdown upregulated the expression of E‐cadherin and decreased that of N‐cadherin and β‐catenin in the SGC7901 gastric cell line . Silencing of SCIN also inhibited the proliferation of human lung carcinoma cells .…”

supporting

confidence: 91%

Loss of scinderin decreased expression of epidermal growth factor receptor and promoted apoptosis of castration‐resistant prostate cancer cells

Lai

Zhao³

et al. 2018

FEBS Open Bio

View full text Add to dashboard Cite

Most patients with prostate cancer will eventually develop the castration‐resistant form characterised by metastasis. Cytoskeleton constituents, including F‐actin, play important roles in maintaining epithelial integrity and their disruption is a major cause of cancer progression. We previously showed that scinderin (SCIN), an important regulator of F‐actin organisation, is highly expressed in poorly differentiated cancer tissues. This study aimed to explore the mechanism of its regulation of cell proliferation. We discovered that SCIN knockdown significantly downregulated epidermal growth factor receptor (EGFR) protein expression, and inhibited epidermal growth factor (EGF)‐mediated cell proliferation and activation of the downstream mitogen‐activated protein kinase kinase (MEK)/extracellular signal‐regulated kinase (ERK) signalling pathway. Silencing of SCIN promoted apoptosis in two cell lines (PC‐3 and DU145), inhibited B‐cell lymphoma‐extra‐large (Bcl‐xl) expression and activated caspase signalling. Furthermore, in vivo studies showed that SCIN deletion slowed tumour growth and decreased EGFR expression. Thus, we conclude that SCIN promotes prostate cancer cell survival by stabilising EGFR and MEK/ERK signalling.

show abstract

supporting

confidence: 91%

Loss of scinderin decreased expression of epidermal growth factor receptor and promoted apoptosis of castration‐resistant prostate cancer cells

Lai

Zhao³

et al. 2018

FEBS Open Bio

View full text Add to dashboard Cite

show abstract

“…As an important actin-binding protein, SCIN participates in actin-capping, -severing and -nucleating. It has been reported that knockdown of SCIN decreases the migratory capability of the highly metastatic GC cell line SGC7901 by promoting the epithelial-mesenchymal transition (EMT) [19]. In the present study, we found that SCIN expression was correlated with the invasion depth and lymph node metastasis of human GC, and associated with decreased survival of patients.…”

Section: Discussionsupporting

confidence: 61%

“…High SCIN expression has also been observed in human lung cancer specimens, and the level of SCIN is associated with cell proliferation in human lung carcinoma cell lines [17]. A quantitative proteomic analysis showed that SCIN was a cisplatin-resistant marker in the HT1376 human bladder cancer cell line [18], and SCIN knockdown effectively reduces cell proliferation and migration in the SGC7901 human GC cell line [19]. However, the clinical significance and the precise mechanisms that control SCIN expression in cancer have not been established.…”

Section: Scin Is Highly Expressed In Both Human Prostate Cancer Specimentioning

confidence: 99%

Scinderin promotes the invasion and metastasis of gastric cancer cells and predicts the outcome of patients

Liu

Chen

et al. 2016

Cancer Letters

View full text Add to dashboard Cite

Invasion and metastasis are major malignant characteristics of human gastric cancer (GC), but the underlying molecular mechanisms are poorly understood. Recent studies have shown that scinderin (SCIN), an actin severing and capping protein that regulates the actin cytoskeleton, is involved in the proliferation and migration of certain cancer cells. Accordingly, this study aimed to investigate the potential role of SCIN in the invasion and metastasis of human GC cells and to evaluate its prognostic value for GC patients. We found that high levels of SCIN expression in GC tumors were correlated with poor overall survival of patients. Silencing of SCIN effectively suppressed the migratory and invasive capabilities of human GC cells in vitro and tumorigenicity and metastasis in vivo. Furthermore, knockdown of SCIN markedly inhibited the formation of filopodia, decreasing GC cell migration and the expression of Cdc42, an important regulator of filopodia by GC cells. These findings suggest that SCIN may be a novel prognostic marker and a potential therapeutic target in human GC.

show abstract

“…In lung and prostate cancer cell lines, SCIN-knockdown was demonstrated to inhibit cell proliferation (10,11), and SCIN was overexpressed in gastric cancer (12). SCIN-knockdown in gastric cell lines decreased the metastatic ability of these cells (13). These results suggest that SCIN may function as an oncogene.…”

Section: Introductionmentioning

confidence: 90%

Scinderin suppresses cell proliferation and predicts the poor prognosis of hepatocellular carcinoma

et al. 2020

View full text Add to dashboard Cite

Hepatocellular carcinoma (HCC) remains an intractable disease despite numerous advancements made in the available treatments over recent decades. Therefore, investigation of the underlying pathogenesis of HCC is urgently required. Our previous microarray result showed that SCIN was generally downregulated in 23 paired tumor/normal tissues. Reverse transcription-quantitative PCR, western blotting and immunohistochemistry were performed in the present study in order to detect the expression of scinderin (SCIN). Lentivirus-mediated gene delivery was used in order to produce SCIN-manipulated cell lines. MTT and crystal violet assays were performed in order to investigate cell growth, and fluorescence-activated cell sorting analysis was used in order to determine cell cycle distribution. SCIN was downregulated in HCC samples, and low SCIN expression predicted the poor prognosis of patients with HCC. Notably, SCIN may have the potential to serve as an independent risk factor for overall survival (3-year overall survival rate of 28.6 and 10.3% in high SCIN expression and low SCIN expression groups, respectively) and disease-free survival (3-year recurrence rate of 71.4 and 84.6% in high SCIN expression and low SCIN expression groups, respectively) in HCC. SCIN inhibited HCC cell proliferation both in vitro and in subcutaneous tumor formation assay. Furthermore, SCIN decreased the levels of phosphorylated STAT3, thereby downregulating cyclin A1 levels in HCC cells. The results of the present study demonstrate the tumor suppressive role of SCIN in HCC, providing a candidate strategy to treat this disease.

show abstract

Suppression of scinderin modulates epithelial-mesenchymal transition markers in highly metastatic gastric cancer cell line SGC-7901

Cited by 17 publications

References 34 publications

Loss of scinderin decreased expression of epidermal growth factor receptor and promoted apoptosis of castration‐resistant prostate cancer cells

Loss of scinderin decreased expression of epidermal growth factor receptor and promoted apoptosis of castration‐resistant prostate cancer cells

Scinderin promotes the invasion and metastasis of gastric cancer cells and predicts the outcome of patients

Scinderin suppresses cell proliferation and predicts the poor prognosis of hepatocellular carcinoma

Contact Info

Product

Resources

About