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LncRNA PTCSC3 is upregulated in osteoporosis and negatively regulates osteoblast apoptosis.

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BMC medical genomics 📖 저널 OA 93.5% 2022: 2/2 OA 2023: 1/1 OA 2024: 1/1 OA 2025: 11/11 OA 2026: 13/15 OA 2022~2026 2022 Vol.15(1) p. 57
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유사 논문
P · Population 대상 환자/모집단
80 patients with osteoporosis (4 clinical stages) and four corresponding groups of healthy controls were enrolled.
I · Intervention 중재 / 시술
추출되지 않음
C · Comparison 대조 / 비교
추출되지 않음
O · Outcome 결과 / 결론
LncRNA PTCSC3 was upregulated in osteoporosis and negatively regulated osteoblast apoptosis. [CONCLUSION] LncRNA PTCSC3 may serve as a potential therapeutic target for osteoporosis.

Liu X, Chen M, Liu Q, Li G, Yang P, Zhang G

📖 무료 전문 🟢 PMC 전문 PMC8925152
📝 환자 설명용 한 줄

[BACKGROUND] It is known that long non-coding RNA (lncRNA) PTCSC3 is involved in thyroid cancer and glioma, but its function in osteoporosis is unknown.

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↓ .bib ↓ .ris
APA Liu X, Chen M, et al. (2022). LncRNA PTCSC3 is upregulated in osteoporosis and negatively regulates osteoblast apoptosis.. BMC medical genomics, 15(1), 57. https://doi.org/10.1186/s12920-022-01182-3
MLA Liu X, et al.. "LncRNA PTCSC3 is upregulated in osteoporosis and negatively regulates osteoblast apoptosis.." BMC medical genomics, vol. 15, no. 1, 2022, pp. 57.
PMID 35296322 ↗

Abstract

[BACKGROUND] It is known that long non-coding RNA (lncRNA) PTCSC3 is involved in thyroid cancer and glioma, but its function in osteoporosis is unknown. The aim of our study was to investigate the role of lncRNA PTCSC3 in osteoporosis.

[METHODS] A total of 80 patients with osteoporosis (4 clinical stages) and four corresponding groups of healthy controls were enrolled. Plasma PTCSC3 levels in the 80 osteoporosis patients and 80 healthy volunteers were measured using RT-qPCR. The diagnostic potential of plasma PTCSC3 for osteoporosis was evaluated by ROC curve analysis with healthy volunteers as the true negative cases and corresponding osteoporosis patients as the true positive cases.

[RESULTS] PTCSC3 was upregulated in osteoporosis patients compared with healthy controls. PTCSC3 levels increased with osteoporosis stages increasing, but not with healthy controls aging. PTCSC3 overexpression separated each stage of osteoporosis from corresponding controls. PTCSC3 overexpression promoted while PTCSC3 silencing inhibited osteoblast apoptosis. However, PTCSC3 overexpression and silencing showed no significant effect on osteoclast apoptosis. LncRNA PTCSC3 was upregulated in osteoporosis and negatively regulated osteoblast apoptosis.

[CONCLUSION] LncRNA PTCSC3 may serve as a potential therapeutic target for osteoporosis.

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