FIP-sch2, a new fungal immunomodulatory protein from Stachybotrys chlorohalonata, suppresses proliferation and migration in lung cancer cells

• DOI: 10.1007/s00253-016-8030-6
• Publication Date: 2017-01-12T00:07:15Z
• Authors: Shuying Li; Zhonghao Jiang; Wenyi Xu; Yingying Xie; Leiming Zhao; Xuanming Tang; Fengzhong Wang; Fengjiao Xin
• Keywords: 0303 health sciences; Lung Neoplasms; Cell Survival; Apoptosis; Real-Time Polymerase Chain Reaction; Recombinant Proteins; 3. Good health; Fungal Proteins; Immunomodulation; 03 medical and health sciences; Stachybotrys; A549 Cells; Cell Movement; Escherichia coli; Humans; Sequence Alignment; Cell Proliferation; Glutathione Transferase

Fungal immunomodulatory protein (FIP)-sch2, an immunomodulatory protein identified in the ascomycete Stachybotrys chlorohalonata by a sequence similarity search, is a novel member of the FIP family. FIP-sch2 shares high sequence identity, structure, and evolutionary conservation with previously reported FIPs. It was satisfactorily expressed in Escherichia coli with a glutathione S-transferase (GST) tag and purified by GST-affinity magnetic beads. To characterize the direct antitumor effects, human lung adenocarcinoma A549 cells were treated with different concentrations of recombinant FIP (rFIP)-sch2 in vitro, and the results showed that rFIP-sch2 could reduce cell viability dose-dependently with a half-maximal inhibitory concentration (IC50) of 9.48 μg/mL. Furthermore, rFIP-sch2 at 8 μg/mL could significantly induce apoptosis and interrupt migration in A549 cells. Notably, the antitumor effect of rFIP-sch2 was equivalent to that of rLZ-8 but was obviously increased compared to rFIP-fve. In addition, the exploration of the antitumor mechanism suggested that rFIP-sch2 induced lung cancer cell death by activating apoptosis and inhibiting migration. Our results indicated that rFIP-sch2 was a promising candidate for use in future cancer therapy.