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In cultured human pulmonary artery smooth muscle cells, hypoxia-promoted cellular viability, DNA synthesis and migration were suppressed by exogenous FSTL1 but enhanced by small interfering RNA targeting FSTL1
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Study suggests that follistatin like 1 plays an important role in lung fibrosis, and may serve as a novel therapeutic target for treatment of silicosis.
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Segmental allergen challenge increases levels of airway follistatin-like 1 in patients with asthma.
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Study found that FSTL1 was downregulated in non-small cell lung cancer (NSCLC) cells. FSTL1 overexpression suppressed tumor cell proliferation, altered cell cycle and induced apoptosis in addition to inhibiting cell survival, migration and invasion. Altogether, results revealed the critical tumor-suppression function of FSTL1 in NSCLC progression, suggesting it as an important factor in NSCLC progression.
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Smad3 knockdown could restore the inhibition of cell proliferation induced by FSTL1 overexpression in MDAMB231FSTL1 cells, indicating that the antiproliferative effect of FSTL1 overexpression may be associated with Smad3 involved TGFbeta signaling pathway regulation. This study identified FSTL1 as an inhibitor of cell proliferation in MDAMB231 and 231BR cell lines
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Dendritic cell-mediated immunity was activated by FSTL1.
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Fstl1serves an important role in liver fibrosis and target deletion of Fstl1 attenuated HSCs activation through suppressing TGFbeta1/Smad3 signaling pathway.
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Results showed that: 1- FSTL-1 expression is localized to the stromal compartment of the pancreas; 2- FSTL-1 expression is reduced in pancreatic cancer, and 3- FSTL-1 inhibited pancreatic cancer cell proliferation.
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Data show that follistatin-like 1 (FSTL1) contributed to unfavorable post-surgical outcome of hepatocellular carcinoma (HCC) patients via inhibiting cell apoptosis.
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results indicate that rs1259293 is associated with an increased risk and unfavorable postoperative prognosis of renal cell carcinoma, possibly by down-regulating FSTL1 expression in renal tissues.
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Data provide evidence that FSTL1 modestly affects the proliferation of breast cancer cells and vascular endothelial cells. These findings improve the understanding of the functions of FSTL1 in breast cancer development and angiogenesis.
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knockdown of FSTL1 inhibited ASM cell proliferation and migration induced by PDGF-BB at least partially via inhibiting the activation of ERK and AKT. These results provide novel insight into the pathogenesis of airway remodeling in childhood asthma and FSTL1 may be a possible therapeutic strategy for the treatment of asthma.
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Fstl1 inhibited Smad1/5/8 phosphorylation by blocking the association between bone morphogenetic protein 4 and Bone Morphogenetic Protein Receptors, Type II via competitive binding to bone morphogenetic protein 4.
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Data show that follistatin like-1 (FSTL1) was frequently downregulated in nasopharyngeal carcinoma (NPC) cell lines and primary tumor biopsies by promoter hypermethylation.
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Results indicate the significance of follistatin-like protein 1 (FSTL1) in driving oncogenesis and metastasis in esophageal squamous cell carcinoma (ESCC) by coordinating NF-kappa B (NFkappaB) and bone morphogenetic proteins (BMP) pathway control.
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FSTL1 mRNA levels increased in castration-resistant prostate cancer in association with predominantly nuclear FSTL1.
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FSTL1 may induce epithelial mesenchymal transition and airway remodeling by activating autophagy.
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DROMs levels positively associated with Fstl1, Hemoglobin A1c and hsCRP levels.
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FSTL1 displays anti-inflammatory effects against oxidized low-density lipoprotein-induced pro-inflammatory cytokine production via a mechanism that involves the TLR4/MyD88/NF-kappaB and MAPK signaling pathways.
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this study shows that 1) the expression of follistatin-like protein 1 is upregulated in rheumatoid arthritis patients; 2) miR-27a inhibits cell migration of rheumatoid arthritis synoviocytes by targeting follistatin-like protein 1 and restraining the TLR4/NFkappaB pathway
