Hydroxysafflor Yellow A Promotes HaCaT Cell Proliferation and Migration by Regulating HBEGF/EGFR and PI3K/AKT Pathways and Circ_0084443.
10.1007/s11655-023-3607-2
- Author:
Yue ZHANG
1
;
Yan-Wei XIAO
1
;
Jing-Xin MA
2
;
Ao-Xue WANG
3
Author Information
1. Department of Dermatology, the Second Hospital of Dalian Medical University, Dalian, Liaoning Province, 116021, China.
2. Department of Cell Biology, Dalian Medical University, Dalian, Liaoning Province, 116044, China.
3. Department of Dermatology, the Second Hospital of Dalian Medical University, Dalian, Liaoning Province, 116021, China. wangaxdl@163.com.
- Publication Type:Journal Article
- Keywords:
circ_0084443;
heparin-binding epidermal growth factor-like growth factor/epidermal growth factor receptor;
hydroxysafflor yellow A;
phosphatidylinositol 3-kinase/protein kinase B
- MeSH:
Humans;
Proto-Oncogene Proteins c-akt/metabolism*;
Phosphatidylinositol 3-Kinase;
Phosphatidylinositol 3-Kinases/metabolism*;
ErbB Receptors/genetics*;
TOR Serine-Threonine Kinases/metabolism*;
Cell Proliferation;
RNA, Messenger/genetics*;
Cell Movement;
Cell Line, Tumor;
Chalcone/analogs & derivatives*;
Quinones
- From:
Chinese journal of integrative medicine
2024;30(3):213-221
- CountryChina
- Language:English
-
Abstract:
OBJECTIVE:To investigate the effect and possible mechanism of hydroxysafflor yellow A (HSYA) on human immortalized keratinocyte cell proliferation and migration.
METHODS:HaCaT cells were treated with HSYA. Cell proliferation was detected by the cell counting kit-8 assay, and cell migration was measured using wound healing assay and Transwell migration assay. The mRNA and protein expression levels of heparin-binding epidermal growth factor (EGF)-like growth factor (HBEGF), EGF receptor (EGFR), phosphatidylinositol 3-kinase (PI3K), protein kinase B (AKT), mammalian target of rapamycin (mTOR), and hypoxia-inducible factor-1α (HIF-1α) were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot, respectively. Circ_0084443-overexpressing HaCaT cells and empty plasmid HaCaT cells were constructed using the lentiviral stable transfection and treated with HSYA. The expression of circ_0084443 was detected by qRT-PCR.
RESULTS:HSYA (800 µmol/L) significantly promoted HaCaT cell proliferation and migration (P<0.05 or P<0.01). It also increased the mRNA and protein expression levels of HBEGF, EGFR, PI3K, AKT, mTOR and HIF-1α, and increased the phosphorylation levels of PI3K and AKT (P<0.05 or P<0.01). Furthermore, HSYA promoted HaCaT cell proliferation and migration via the HBEGF/EGFR and PI3K/AKT/mTOR signaling pathways (P<0.01). Circ_0084443 attenuated the mRNA expression levels of HBEGF, EGFR, PI3K, AKT, mTOR and HIF-1α (P<0.05). HSYA inhibited the circ_0084443 expression, further antagonized the inhibition of circ_0084443 on HBEGF, EGFR, PI3K, AKT, mTOR and HIF-1α, and promoted the proliferation of circ_0084443-overexpressing HaCaT cells (P<0.05 or P<0.01). However, HSYA could not influence the inhibitory effect of circ_0084443 on HaCaT cell migration (P>0.05).
CONCLUSION:HSYA played an accelerative role in HaCaT cell proliferation and migration, which may be attributable to activating HBEGF/EGFR and PI3K/AKT signaling pathways, and had a particular inhibitory effect on the keratinocyte negative regulator circ_0084443.
