Melittin Constrains the Expression of Identified Key Genes Associated with Bladder Cancer

Abstract

This work is aimed at investigating the effect of melittin on identified key genes in bladder cancer (BC) and further providing a theoretical basis for BC treatment. GSE35014 downloaded from the Gene Expression Omnibus (GEO) database was used to screen differentially expressed genes (DEGs) in BC cells and control. Results showed that a total of 389 upregulated and 169 downregulated genes were identified. Subsequently, GO analysis, KEGG pathway enrichment analysis, and PPI network analysis were employed to disclose the crucial genes and signaling pathways involved in BC. Fifteen module-related DEGs and their associated signaling pathways were obtained according to the PPI network and modular analyses. Based on the analysis of articles retrieved in the PubMed database, we found that melittin could induce apoptosis and constrain the progression of tumor cells as a result of regulating critical cancer-related signaling pathways, such as PI3K-Akt and TNF signaling pathways. Furthermore, PI3K-Akt and TNF signaling pathways were also found to be associated with module-related DEGs according to biological analyses. At last, qRT-PCR analysis demonstrated that melittin could constrain the expression of module-related DEGs (LPAR1, COL5A1, COL6A2, CXCL1, CXCL2, and CXCL3) associated with PI3K-Akt and TNF signaling pathways in BC cells. Functional assays revealed that melittin could constrain the proliferative and migrated abilities of BC cells. Conjointly, these findings provide a theoretical basis for these six genes as drug-sensitive markers of melittin in BC treatment.

Melittin inhibits proliferation, migration and invasion of bladder cancer cells by regulating key genes based on bioinformatics and experimental assays

“…In the present study, both the scratch wound‐healing and transwell assays were employed to detect cell migration. The scratch wound‐healing assay was performed as previously reported . The initial gap length at 0 hours and residual gap length at 24 hours after wounding were calculated from photomicrographs.…”

“…The scratch woundhealing assay was performed as previously reported. 16 The initial gap length at 0 hours and residual gap length at 24 hours after wounding were calculated from photomicrographs. The transwell assay was performed in 24-well Boyden chambers (Corning Inc) pre-coated with the absence of Matrigel (BD Biosciences), as previously described.…”

“…In 1998, Winder et al demonstrated that MEL contributed to a complete loss of tumorigenicity in certain clones and reduced tumorigenicity in a human BC‐derived cell line. However, Jin et al presented evidence that MEL constrained the proliferative and migratory abilities of BC cells. The specific mechanism of MEL affecting BC and its potential use in anti‐BC therapy is worthy of investigation.…”

Long non‑coding RNA ADAMTS9‑AS2 inhibits liver cancer cell proliferation, migration and invasion

“…The expression levels of ADAMTS9-AS2 and ADAMTS9 were detected via RT-qPCR as described previously ( 19 ). Briefly, total RNA was extracted from cells using TRIzol ® reagent (Thermo Fisher Scientific, Inc.) according to the manufacturer's instructions.…”

An overview of the bioactive compounds, therapeutic properties and toxic effects of apitoxin

“…This compound is also cytotoxic against cancer cells among other mechanisms through the activation of apoptotic pathways (both caspase-dependent and caspase-independent) and PLA 2 pathways (Lee et al, 2018;Jin et al, 2018;Shin et al, 2017;Zhang and Chen, 2017;Wang et al, 2017). Indeed, the growth inhibitory potential and the capacity to suppress tumour metastasis of MLT has been observed in several types of cancer cells like liver, renal, prostate, breast, lung, bladder, gastric and leukemia, suggesting that it may be a potent agent to use in chemotherapy (Liu et al, 2016;Moreno and Giralt, 2015;Kong et al, 2016).…”