Huaier Inhibits Cancer Progression Correlated with the Mutated EGFR and Other Receptor Tyrosine Kinases (c-MET/erbB-2) by Down-Regulation of Multiple Signal Transduction Pathways

Author(s): Manami Tanaka, Tomoo Tanaka, Fei Teng, Hong Lin, Ning Li, Zhu Luo, Ding Wei, and Zhengxin Lu

Background: Clinical significance of anti-cancer effects of Huaier (Trametes robiniophila murr) has been emphasized recently [1-3]. We have already reported the successful Huaier therapy based on the individual genomic potential and miRNA-mediated transcription control [4-7]. In prostate cancer, Huaier also proved to have a significant efficacy on the prevention of cancer progression [6].

Objective: We have been initiating clinical research for thorough understanding of molecular basis of Huaier effects, which contributes to define the responsible molecules and biosystems not only for recovery, but also for prevention of cancer progression and tumorigenesis.

Methods: The peripheral blood samples from the volunteer patients were analyzed by total RNA and non-coding small RNA sequencing on BGISEQ-500 Platform [8, 9]. KEGG pathway classification was hired for the analysis of the obtained information in the present study ( [10].

Results: In the present study, we focused on the patient and her family correlated with the mutated EGFR [11] and other receptor tyrosine kinases (c-MET [12-14]/erbB-2 [15, 16]). At first, high ratio of SNP variants as A-G transitions (241,896 in total, 37.0%) and A-C transversions (43,213 in total, 6.5 %), with skipped-exon (51%), which influenced significant changes in transcriptional factors and corresponding gene expression in multiple signal transduction pathways. The ratio of alteration ranged from 10% to 30% of total number of transcripts, detected as a drastic down-regulation by Huaier administration. Although the patient was diagnosed as benign meningioma, there were no genomic alteration in RNA polymerase II and its subunits [17], but only quantitative down-regulation in the attached transcriptional fac

© 2016-2024, Copyrights Fortune Journals. All Rights Reserved