2024년
2024 한국질량분석학회 여름학술대회 및 총회
2024. 08.28 (수) ~ 2024. 08.30 (금)
군산새만금컨벤션센터(GSCO)
초록검색
| 제목 | Lipidomic and metabolomic profiling associated with drug resistance in chronic myeloid leukemia cells |
|---|---|
| 작성자 | 장서영 (한국기초과학지원연구원) |
| 발표구분 | 포스터발표 |
| 발표분야 | 4. Medical / Pharmaceutical Science |
| 발표자 |
장서영 (한국기초과학지원연구원) |
| 주저자 | 장서영 (한국기초과학지원연구원) |
| 교신저자 |
황금숙 ( 한국기초과학지원연구원) |
| 저자 |
장서영 (한국기초과학지원연구원) 황금숙 ( 한국기초과학지원연구원) |
|
Chronic myeloid leukemia (CML) is caused by abnormal proliferation of hematopoietic stem cells and has primarily been treated by imatinib (IM) as a tyrosine kinase inhibitor. HMGCLL1 located in 6p12.1 is a predictive genetic biomarker for deep molecular response to IM therapy in CML patients. However, no mechanistic studies have examined the role of HMGCLL1 associated with drug resistance in CML cells. Herein, we
investigate the metabolic response to inhibiting HMGCLL1 in cells using
metabolomic, lipidomic, and isotope-tracing analyses. We found that the
inhibition of HMGCLL1 enriches metabolites relevant to amino acid metabolism.
Moreover, lipidomic analysis shows that the blockade of HMGCLL1 increases the
free fatty acid and polyunsaturated fatty acid (PUFA)-containing phospholipid
species, and reduces lysophospholipid species. Using isotope-tracing analyses,
we confirmed that inhibition of HMGCLL1 does not upregulate PUFA biosynthesis. |
|