Upregulation of autophagy by Ginsenoside Rg2 in MCF-7 cells

Autophagy is a major intracellular degradation process that plays an important role in cell survival, stress responses, nutrient sensing and development. Our previous studies have shown that Rg2, a triterpenoid saponin contained in ginseng, protects cells against UVB-induced genotoxicity by increasing DNA repair, in possible association with modulation of protein levels involved in p53 pathway. In this study, we determined an upregulation of autophagy by Rg2. Rg2 treatment for 24 h in MCF-7, a breast cancer cell, did not show cytotoxicity up to 200 mu M. Rg2 also upregulated the level of p-p53, p-AMPK, p-ACC, Atg-7 and LC3-II and decreased the level of p62 in concentration-dependent manners. We also determined the level of p53, AMPK, p62, Atg-7 and LC3 after UVB exposure and subsequent incubation in growth medium for 24 h. UVB increased the level of p-p53, p-AMPK, p-ACC and decreased the levels of p62, Atg-7 and LC3-II. Interestingly, Rg2 treatment for 24 h after UVB exposure increased the levels of p-p53, p-AMPK, p-ACC, Atg-7 and LC3-II and decreased the level of cyclobutane pyrimidine dimer, a UVB-induced DNA damage in concentration-dependent manners. All these results suggest that Rg2 increased autophagy and decreased UVB-induced DNA damage, in possible association with the modulation of protein levels in p53- and autophagic pathways

Genetic Mapping of Resistance Sources against ChiVMV (Chili veinal mottle virus) in Hot Pepper

Chili veinal mottle virus (ChiVMV) is the notorious virus affecting the severe loss of pepper production in Asia and Africa. To map the positions of ChiVMV resistance genes, F2 mapping populations were constructed by crossing each resistance accession, Capsicum annuum, 'CV3', 'CV4', and 'CV8' with susceptible C. annuum, 'Jeju'. In the 'CV3' and 'CV8' mapping populations, resistance genes were inherited by a single dominant manner and located to the short arm of pepper chromosome 6. The ChiVMV resistance marker reported in the previous study was cosegregated with these genes. Through allelism test of resistance genes from 'CV3' and 'CV8', it was revealed that the resistance gene in each line was originated from the same locus, and we named this gene, Cvr1 (ChiVMV resistance 1) locus. We developed several SNP markers linked to Cvr1 using pepper genome information and pepper bacterial artificial chromosome (BAC) sequences. By contrast, the inheritance mode of ChiVMV resistance in CV4 was different from those of CV3 or CV8. The inheritance study showed that two independent complementary genes involved in ChiVMV resistance in CV4. To map the resistance genes in CV4, SNP-based linkage map was constructed by genotyping-by-sequencing (GBS) method. The result of this study will accelerate the ChiVMV resistance research and breeding resistance cultivar to ChiVMV in pepper.OAIID:RECH_ACHV_DSTSH_NO:A201625341RECH_ACHV_FG:RR00200003ADJUST_YN:EMP_ID:A076900CITE_RATE:FILENAME:이종호_2016육종학회.pdfDEPT_NM:식물생산과학부EMAIL:[email protected]_YN:FILEURL:https://srnd.snu.ac.kr/eXrepEIR/fws/file/41c0cd80-34f4-45cc-bf33-0bb81b69ca1d/linkCONFIRM:

Microtubule Acetylation Controls MDA-MB-231 Breast Cancer Cell Invasion through the Modulation of Endoplasmic Reticulum Stress

During aggressive cancer progression, cancer cells adapt to unique microenvironments by withstanding various cellular stresses, including endoplasmic reticulum (ER) stress. However, the mechanism whereby cancer cells overcome the ER stress to survive remains to be elucidated. Herein, we demonstrated that microtubule acetylation in cancer cells grown on a stiff matrix promotes cancer progression by preventing excessive ER stress. Downregulation of microtubule acetylation using shRNA or CRSIPR/Cas9 techniques targeting ATAT1, which encodes α-tubulin N-acetyltransferase (αTAT1), resulted in the upregulation of ER stress markers, changes in ER morphology, and enhanced tunicamycin-induced UPR signaling in cancer cells. A set of genes involved in cancer progression, especially focal adhesion genes, were downregulated in both ATAT1-knockout and tunicamycin-treated cells, whereas ATAT1 overexpression restored the gene expression inhibited by tunicamycin. Finally, the expression of ATAT1 and ER stress marker genes were negatively correlated in various breast cancer types. Taken together, our results suggest that disruption of microtubule acetylation is a potent therapeutic tool for preventing breast cancer progression through the upregulation of ER stress. Moreover, ATAT1 and ER stress marker genes may be useful diagnostic markers in various breast cancer types