<p>Up-Regulation of FSTL3, Regulated by lncRNA DSCAM-AS1/miR-122-5p Axis, Promotes Proliferation and Migration of Non-Small Cell Lung Cancer Cells</p>

Abstract

Background: Follistatin-like 3 (FSTL3) binds and inactivates activin, a growth factor with cell growth and differentiation. Previous studies reported that it is overexpressed in invasive breast cancers, and its expression and function in non-small cell lung cancer (NSCLC) remain unclear. Materials and Methods: Immunohistochemistry was employed to probe the expression of FSTL3 in NSCLC tissues. Real-time PCR (RT-PCR) was applied to detect the expression of lncRNA DSCAM-AS1 and miR-122-5p. A549 cells and H1299 cells were used as cell models. The biological influence of FSTL3 on cells was studied using CCK-8 assay, wound healing assay and transwell assay in vitro, respectively. In vivo subcutaneous xenotransplanted tumor model and tail vein injection model in mice were also constructed to validate the roles of FSTL3. Interactions between miR-122-5p and FSTL3, DSCAM-AS1 and miR-122-5p were determined by bioinformatics analysis, RT-PCR, and dual-luciferase reporter assay. Results: FSTL3 and DSCAM-AS1 were remarkably up-regulated in NSCLC samples, and miR-122-5p was down-regulated. FSTL3 was associated with worse prognosis of NSCLC patients. FSTL3 knockdown markedly inhibited the viability, migration and invasion of NSCLCs in vitro and in vivo. DSCAM-AS1 could down-regulate miR-122-5p via sponging it, and FSTL3 was a target gene of miR-122-5p. Conclusion: Taken together, our study identified that FSTL3 was a new oncogene of NSCLC, which was regulated by DSCAM-AS1 and miR-122-5p. These findings suggested that FSTL3, DSCAM-AS1 and miR-122-5p might serve as a new valuable therapeutic target for NSCLC.

Follistatin-Like 3 Correlates With Lymph Node Metastasis and Serves as a Biomarker of Extracellular Matrix Remodeling in Colorectal Cancer

“…FSTL3, i.e., follistatin-like 3, is a secreted glycoprotein that is physiologically released by adipose tissue, reproductive, glands, liver, heart, and especially placenta. Recently, significant overexpression was also found in some malignant tumors (25,45,46). FSLT3 expression has been shown to be significantly associated with LNM and worse outcomes in patients with nonsmall cell lung cancer cell and thyroid cancer (25,45).…”

“…IHC staining of paraffin-embedded tissues with antibody against FSTL3 (1:25; Absin, abs101405, Shanghai, China) was performed according to standard procedures as previously described (25), and scores were recorded. The expression level of FSTL3 is evaluated according to the total histochemical score, which is calculated as the product of staining intensity and the positive cell proportion.…”

Genomics and prognosis analysis of epithelial-mesenchymal transition in colorectal cancer patients

“…FSTL3 was upregulated by the lncRNA DSCAM-AS1/miR-122-5p axis and could promote proliferation and migration of non-small cell lung cancer cells [ 39 ]. Moreover, FSTL3 served as a surrogate marker in breast cancer and was the only variable that could distinguish a benign breast mass from a malignant one [ 40 ].…”

Investigation of the underlying hub genes and molecular pathogenesis in gastric cancer by integrated bioinformatic analyses

“…Enriched up regulated genes such as COL4A2 [153], ITGA11 [154], LAMA5 [155], COL5A2 [156], ADAMTS4 [157], ADAMTS14 [158], ANXA13 [159], HTRA3 [160] and ADAMTS12 [161] were responsible for invasion of various types of cancer cells, but these genes may be associated with invasion of GC cells. Enriched up regulated genes such as COMP (cartilage oligomeric matrix protein) [162], TNC (tenascin C) [163], ITGB8 [164], FSTL3 [165] and PLXNA1 [166] were important for proliferation of many cancer cells types, but these genes may be liable for proliferation of GC cells. High expression of enriched genes such as COL3A1 [167], COL5A1 [168], COL7A1 [169], COL8A1 [170], CTSB (cathepsin B)…”