Zhang Liubing, Peng Aiping, Qin Yue
Department of Medical Laboratory, Longhua District People's Hospital, Shenzhen, 518100, China.
Department of Nephrology, Longhua District People's Hospital, Shenzhen, 518100, China.
Discov Oncol. 2025 May 30;16(1):955. doi: 10.1007/s12672-025-02767-x.
To examine the expression of non-SMC condensin II complex subunit D3 (NCAPD3) in papillary thyroid carcinoma (PTC) tissues, assess its impact on the growth and metastatic potential of PTC cells, and investigate its role in regulating glycolysis to uncover the underlying mechanisms involved.
NCAPD3 levels in PTC tissues were detected using immunohistochemistry. siRNA transfection was used to silence NCAPD3 in K1 and TPC-1 cells. Cell proliferation rates were detected using the Cell Counting Kit-8 assay, migration rates were evaluated using wound healing and Transwell cell migration assays, and invasion rates were assessed using the Transwell-Matrigel cell invasion assay. Moreover, the aerobic glycolysis-related factors lactate, lactate dehydrogenase A (LDHA), and pyruvate kinase M2 (PKM2) were detected using kits.
NCAPD3 was highly expressed in PTC tissues. Its expression showed no significant association with patient age, gender, or lymphocytic thyroiditis but was significantly correlated with larger tumor size and lymphovascular invasion. NCAPD3 expression significantly decreased in K1 and TPC-1 cells after transfection with siRNA. Low NCAPD3 expression reduced the proliferation rate of K1 and TPC-1 cells and inhibited cell migration and invasion. Moreover, NCAPD3 silencing decreased LDHA, PKM2, and lactate levels.
NCAPD3 was highly expressed in PTC tissues, and correlated with aggressive features (tumor size and lymphovascular invasion). NCAPD3 silencing inhibited proliferation, migration, invasion, and aerobic glycolysis of PTC cells. Therefore, NCAPD3 may serve as a potential therapeutic target for PTC.
检测非SMC凝聚素II复合物亚基D3（NCAPD3）在甲状腺乳头状癌（PTC）组织中的表达，评估其对PTC细胞生长和转移潜能的影响，并研究其在调节糖酵解中的作用，以揭示潜在机制。
采用免疫组织化学法检测PTC组织中NCAPD3水平。利用小干扰RNA（siRNA）转染使K1和TPC-1细胞中的NCAPD3沉默。使用细胞计数试剂盒-8检测细胞增殖率，采用伤口愈合实验和Transwell细胞迁移实验评估细胞迁移率，运用Transwell-基质胶细胞侵袭实验评估细胞侵袭率。此外，使用试剂盒检测有氧糖酵解相关因子乳酸、乳酸脱氢酶A（LDHA）和丙酮酸激酶M2（PKM2）。
NCAPD3在PTC组织中高表达。其表达与患者年龄、性别或淋巴细胞性甲状腺炎无显著相关性，但与肿瘤较大尺寸和淋巴管侵犯显著相关。转染siRNA后，K1和TPC-1细胞中NCAPD3表达显著降低。低NCAPD3表达降低了K1和TPC-1细胞的增殖率，并抑制细胞迁移和侵袭。此外，NCAPD3沉默降低了LDHA、PKM2和乳酸水平。
NCAPD3在PTC组织中高表达，并与侵袭性特征（肿瘤大小和淋巴管侵犯）相关。NCAPD3沉默抑制了PTC细胞的增殖、迁移、侵袭和有氧糖酵解。因此，NCAPD3可能成为PTC的潜在治疗靶点。
