Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.6.3.44 (
P-glycoprotein
)
13,344
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Standard therapy strategies for cervical cancer (CC) typically are centered on cisplatin (DDP)-based chemotherapy, while the effects of PSAT1 on cisplatin resistance in CC have not been elucidated. Cisplatin-resistant CC cell line of SiHa (SiHa-R) was established and short hairpin RNA (shRNA) targeting PSAT1 was generated to evaluate the effect of PSAT1 knockdown on CC progression. Cell viability and apoptosis were examined by using CCK-8 and flow cytometry assays. The protein levels of p-Akt, t-Akt, PCNA, cleaved caspase-3,
P-glycoprotein
(
P-gp
), and multidrug resistance related protein (MRP)-1 were assessed by western blotting. Cisplatin-resistant CC cells (SiHa-R) exhibited higher expression level of PSAT1 rather than parental SiHa cells. PSAT1 knockdown lowered the IC
50
of cisplatin, inhibited the colony formation numbers, and facilitated the apoptosis ability in SiHa-R cells. PSAT1 knockdown also suppressed the protein levels of phospho-Akt, proteins involved in proliferation (PCNA) and drug resistance (
P-gp
and MRP-1), increased
apoptosis related protein
(cleaved caspase-3), while the PI3K/Akt agonist, 740 Y-P, markedly reversed these above effects. Inhibition of PSAT1 reduced cisplatin resistance in SiHa-R cells through suppressing proliferation and inducing apoptosis by blocking PI3K/Akt signaling pathway. PSAT1 may be a potential therapeutic target to reverse chemoresistance in cisplatin-resistant CC.
...
PMID:PSAT1 Upregulation Contributes to Cell Growth and Cisplatin Resistance in Cervical Cancer Cells via Regulating PI3K/AKT Signaling Pathway. 3282 49
