These data suggest that Cx43 inhibits the invasion and metastasis of pulmonary giant cell carcinoma cells by modulating the secretion of FSTL1, which is regulated by histone acetylation.

the knockdown of FSTL1 induces apoptosis through a mitotic arrest and caspase-dependent cell death. FSTL1 plays the important roles in cellular proliferation and apoptosis in lung cancer cells, and thus can be a new target for lung cancer treatment.

current study revealed that low FSTL1, BMP4, and Smad4 expression significantly predict poor prognosis in lung adenocarcinoma but not in squamous cell carcinoma.

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.

expression of DIP2A (the receptor of FSTL1) in tumor cells is critical for FSTL1-induced neoplastic immune resistance; FSTL1/DIP2A co-positivity in non-small-cell lung tumor (NSCLC) tissues correlates with poor prognosis in NSCLC patients.

Reduced levels of FSTL1 were detected in various tumors and were associated with poor clinical outcome in patients with non-small cell lung cancer. FSTL1 expression negatively correlated with the metastatic potential of lung cancer cells. FSTL1 directly bound to the proform of SPP1/osteopontin, restraining proteolytic activation of SPP1, which led to inactivation of integrin/CD44-associated signaling.