1. A novel class of antimicrobial peptides from the scorpion Heterometrus spinifer
Yao Nie, Xian-Chun Zeng, Ye Yang, Feng Luo, Xuesong Luo, Shifen Wu, Lei Zhang, Jianping Zhou Peptides. 2012 Dec;38(2):389-94. doi: 10.1016/j.peptides.2012.09.012. Epub 2012 Sep 21.
The venom peptides from the scorpion Heterometrus spinifer have been poorly characterized so far. Here, we identified a novel class of antimicrobial peptides from the venom gland of H. spinifer, which were referred to as HsAp, HsAp2, HsAp3 and HsAp4, respectively. Each of the four peptides consists of 29 amino acid residues, and is cationic and weakly amphipathic. They display no significant homology to any other known peptides, and thus represent a new family of venom peptides from scorpions. Antimicrobial assay showed that HsAp is able to inhibit the growth of both Gram-negative and Gram-positive bacteria with the MIC values of 11.8-51.2 μM. HsAp is also able to inhibit the growth of the tested fungus. Genomic analysis indicated that the genes of all the four peptides are intronless. Our studies expand the families of antimicrobial peptides from scorpions.
2. Inhibition of DNAJC12 Inhibited Tumorigenesis of Rectal Cancer via Downregulating HSPA4 Expression
Qi Sun, Yan Lv, Weihua Sun Evid Based Complement Alternat Med. 2022 Sep 21;2022:1027895. doi: 10.1155/2022/1027895. eCollection 2022.
Background: Dysregulation of DnaJ heat shock protein family (HSP40) member C12 (DNAJC12) is implicated in the malignancy progression of multiple cancers. The current study aimed to determine the biology function and mechanism of DNAJC12 in rectal cancer (RC). Methods: RC tissues, adjacent tissues, RC cell lines, and normal colorectal epithelial cell lines were collected to analyze DNAJC12 expression. The abilities of DNAJC12 on proliferation, migration, and apoptosis of RC cells were detected by CCK-8, wound healing, and flow cytometry assays. Co-IP assays were carried out to confirm the association between DNAJC12 and HSPA4. The effect of DNAJC12 on tumor growth was detected by using the xenograft model of nude mice. Results: Elevation of DNAJC12 was uncovered in RC tissues and cell lines. DNAJC12 upregulation facilitated RC cell proliferation and migration and induced apoptosis, while DNAJC12 interference showed the opposite results. Besides, HSAP4 served as a potential binding protein for DNAJC12. Rescue experiments revealed that elevated of HSAP4 restored the impact of DNAJC12 silencing on the cell functions. Finally, DNAJC12 silencing hampered tumor growth of RC in vivo. Conclusion: In summary, this study highlighted a key player of DNAJC12 in modulating the malignant biological progression of RC via DNAJC12/HSPA4 axis, displaying a potential therapeutic target for RC.
3. Whole exome sequencing and system biology analysis support the "two-hit" mechanism in the onset of Ameloblastoma
Y Shi, M Li, Y Yu, Y Zhou, S Wang Med Oral Patol Oral Cir Bucal. 2021 Jul 1;26(4):e510-e517. doi: 10.4317/medoral.24385.
Background: Ameloblastoma is the most frequent odontogenic tumor. Various evidence has highlighted the role of somatic mutations, including recurrent mutation BRAF V600E, in the tumorigenesis of Ameloblastoma, but the intact genetic pathology remains unknown. Material and methods: We sequenced the whole exome of both tumor tissue and healthy bone tissue from four mandibular ameloblastoma patients. The identified somatic mutations were integrated into Weighted Gene Co-expression Network Analysis on publicly available expression data of odontoblast, ameloblast, and Ameloblastoma. Results: We identified a total of 70 rare and severe somatic mutations. We found BRAF V600E on all four patients, supporting previous discovery. HSAP4 was also hit by two missense mutations on two different patients. By applying Weighted Gene Co-expression Network Analysis on expression data of odontoblast, ameloblast, and Ameloblastoma, we found a proliferation-associated gene module that was significantly disrupted in tumor tissues. Each patient carried at least two rare, severe somatic mutations affecting genes within this module, including HSPA4, GNAS, CLTC, NES, and KMT2D. All these mutations had a ratio of variant-support reads lower than BRAF V600E, indicating that they occurred later than BRAF V600E. Conclusions: We suggest that a severe somatic mutation on the gene network of cell proliferation other than BRAF V600E, namely second hit, may contribute to the tumorigenesis of Ameloblastoma.
