Abstract
Metastasis is a crucial impediment to the successful treatment for gastric cancer. SPOCK1 has been demonstrated to facilitate cancer metastasis in certain types of cancers; however, the role of SPOCK1 in the invasion and metastasis of gastric cancer remains elusive. SPOCK1 and epithelial‐mesenchymal transition (EMT)‐related biomarkers were detected by immunohistochemistry and Western blot in gastric cancer specimens. Other methods including stably transfected against SPOCK1 into gastric cancer cells, Western blot, migration and invasion assays in vitro and metastasis assay in vivo were also performed. The elevated expression of SPOCK1 correlates with EMT‐related markers in human gastric cancer tissue, clinical metastasis and a poor prognosis in patients with gastric cancer. In addition, knockdown of SPOCK1 expression significantly inhibits the invasion and metastasis of gastric cancer cells in vitro and in vivo, inversely, SPOCK1 overexpression results in the opposite effect. Interestingly, SPOCK1 expression has no effect on cell proliferation in vitro and in vivo. Regarding the mechanism(s) of SPOCK1‐induced cells invasion and metastasis, we prove that Slug‐induced EMT is involved in SPOCK1‐facilitating gastric cancer cells invasion and metastasis. The elevated SPOCK1 expression is closely correlated with cancer metastasis and patient survival, and SPOCK1 promotes the invasion and metastasis of gastric cancer through Slug‐mediated EMT, thereby possibly providing a novel therapeutic target for gastric cancer.
Highlights
Gastric cancer is the fifth most common malignancy and is the third leading cause of cancer-related deaths worldwide [1, 2]
We demonstrated a significant positive correlation between high expression of SPOCK1 in primary lesion and poor prognosis in patients with gastric cancer, and a conclusion that SPOCK1 contributed to the invasion and metastasis of gastric cancer via Slug-mediated epithelial-mesenchymal transition (EMT)
SPOCK1 in AGS cells showed the opposite effect (Fig. 5F). These results demonstrate that SPOCK1 facilitates the invasion and metastasis of gastric cancer cells via inducing EMT
Summary
Gastric cancer is the fifth most common malignancy and is the third leading cause of cancer-related deaths worldwide [1, 2]. Considering the high probability of metastasis and recurrence and a deficiency of effective therapeutic strategies for patients with advanced gastric cancer during past decades, patients are much more susceptible to a poor prognosis even after a comprehensive therapy [3]. The molecular mechanisms responsible for the invasion and metastasis of gastric cancer remain poorly characterized. Identification of novel metastases-related genes and elaboration of the underlying mechanism(s) may provide potential targets for anticancer metastasis treatment. Recent investigations have revealed that cancer cell activation of EMT contributes to cell invasion and metastasis in multiple cancers [4, 5].
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