|
|
|
| Effect of T3 on proliferation of papillary carcinoma of thyroid cells TPC-1 and its mechanism#br# |
| CHENG Yanan WANG Yan SUN Rongxin LANG Jianan CAO Bin YANG Longyan ZHAO Dong |
| Center for Endocrinology, Metabolism, and Immune Diseases, Beijing Luhe Hospital, Capital Medical University, Beijing 101149, China |
|
|
|
Abstract Objective To investigate the effect of triiodothyronine (T3) on proliferation of papillary carcinoma of thyroid cells TPC-1 and its mechanism. Methods TPC-1 cells were divided into control group (0 ng/ml T3 treatment group), 12.5 ng/ml T3 treatment group and 50 ng/ml T3 treatment group, and treated with corresponding T3 concentration, respectively. Real-time unlabeled cell function analysis technique (RTCA) and clonal formation assay were used to detect the proliferation ability of the cells, and Western blot was used to detect the expression level of PDZK1 in the cells. TPC-1 cells were divided into knockout PDZK1 (shPDZK1) group, knockout control (shNC) group, overexpression PDZK1 (PDZK1) group and overexpression control (Vector) group by lentivirus transfection method. The expression level of PDZK1 in TPC-1 cells was detected by Western blot. Meanwhile, cells in each group were treated with different concentrations of T3 (0, 12.5, 50 ng/ml), and the clonal formation ability of cells was detected by clonal formation assay. Results The cell index and clone formation number of TPC-1 in 12.5 and 50 ng/ml T3 treatment groups were significantly higher than those in control group, and the differences were highly statistically significant (P ＜ 0.01). The expression levels of PDZK1 in 12.5 and 50 ng/ml T3 treatment groups were significantly higher than that in control group, and the differences were statistically significant (P ＜ 0.05 or P ＜ 0.01). Compared with shNC group, the expression level of PDZK1 in shPDZK1 group was significantly lower, and the difference was statistically significant (P ＜ 0.05). Compared with the Vector group, the expression level of PDZK1 in the PDZK1 group was significantly increased, and the difference was highly statistically significant (P ＜ 0.01). Compared with the shNC group, the clore formation number in the shPDZK1 group was significantly decreased after T3 treatment of 0, 12.5, and 50 ng/ml, and the differences were statistically significant (P ＜ 0.05 or P ＜ 0.01). Compared with Vector group, the clone formation number in PDZK1 group was significantly increased in 0, 12.5, and 50 ng/ml T3 treatments, and the differences were statistically significant (P ＜ 0.05 or P ＜ 0.01). Conclusion T3 may regulate TPC-1 cell proliferation by up-regulating PDZK1 expression.
|
|
|
|
|
|
[1] Li R，Wang Y，Du L. A rapidly increasing trend of thyroid cancer incidence in selected East Asian countries：Joinpoint regression and age-period-cohort analyses [J]. Gland Surg，2020，9（4）：968-984.
[2] Sui C，Liang N，Du R，et al. Time trend analysis of thyroid cancer surgery in China：single institutional database analysis of 15，000 patients [J]. Endocrine，2020，68（3）：617-628.
[3] Pastor■i■ Grgi■ M，Stubljar B，Per?觢e P，et al. Total Thyroidectomy with Central Node Dissection is a Valuable Option in Papillary Thyroid Cancer Treatment [J]. ActaClin Croat，2020，59（Suppl 1）：102-107.
[4] Abdullah MI，Junit SM，Ng KL，et al. Papillary Thyroid Cancer：Genetic Alterations and Molecular Biomarker Investigations [J]. Int J Med Sci，2019，16（3）：450-460.
[5] Liu F，Zhu Y，Qian Y，et al. Effects of gold nanorods modified with antiepidermal growth factor receptor monoclonal antibody on laryngeal cancer cells [J]. Turk J Biol，2018， 42（2）：144-151.
[6] Foster JR，Tinwell H，Melching-Kollmuss S. A review of species differences in the control of，and response to，chemical-induced thyroid hormone perturbations leading to thyroid cancer [J]. Arch Toxicol，2021，95（3）：807-836.
[7] Tsui KH，Hsieh WC，Lin MH，et al. Triiodothyronine modulates cell proliferation of human prostatic carcinoma cells by downregulation of the B-cell translocation gene 2 [J]. Prostate，2008，68（6）：610-619.
[8] Meng R，Tang HY，Westfall J，et al. Crosstalk between integrin αvβ3 and estrogen receptor-α is involved in thyroid hormone-induced proliferation in human lung carcinoma cells [J]. PLoS One，2011，6（11）：e27547.
[9] Zhang L，Zhang F，Li Y，et al. Triiodothyronine Promotes Cell Proliferation of Breast Cancer via Modulating miR-204/Amphiregulin [J]. Pathol Oncol Res，2019，25（2）：653-658.
[10] Ferreira C，Prestin K，Hussner J，et al. PDZ domain containing protein 1（PDZK1），a modulator of membrane proteins，is regulated by the nuclear receptor THRβ[J]. Mol Cell Endocrinol，2018，461：215-225.
[11] Tao T，Yang X，Zheng J，et al. PDZK1 inhibits the development and progression of renal cell carcinoma by suppression of SHP-1 phosphorylation [J]. Oncogene，2017， 36（44）：6119-6131.
[12] Gild ML，Tsang VHM，Clifton-Bligh RJ，et al. Multikinase inhibitors in thyroid cancer：timing of targeted therapy [J]. Nat Rev Endocrinol，2021，17（4）：225-234.
[13] Berinde GM，Socaciu AI，Socaciu MA，et al. Thyroid Cancer Diagnostics Related to Occupational and Environmental Risk Factors：An Integrated Risk Assessment Approach [J]. Diagnostics （Basel），2022，12（2）：318.
[14] Wang TS，Sosa JA. Thyroid surgery for differentiated thyroid cancer-recent advances and future directions [J]. Nat Rev Endocrinol，2018，14（11）：670-683.
[15] Xing M. BRAF mutation in papillary thyroid cancer：pathogenic role，molecular bases，and clinical implications [J]. Endocr Rev，2007，28（7）：742-762.
[16] Cheng SY，Leonard JL，Davis PJ. Molecular aspects of thyroid hormone actions [J]. Endocr Rev，2010，31（2）：139-170.
[17] Kowalik MA，Puliga E，Cabras L，et al. Thyroid hormone inhibits hepatocellular carcinoma progression via induction of differentiation and metabolic reprogramming [J]. J Hepatol， 2020，72（6）：1159-1169.
[18] Lin HY，Tang HY，Shih A，et al. Thyroid hormone is a MAPK-dependent growth factor for thyroid cancer cells and is anti-apoptotic [J]. Steroids. 2007，72（2）：180-187.
[19] Perri A，Catalano S，Bonofiglio D，et al. T3 enhances thyroid cancer cell proliferation through TRβ1/Oct-1-mediated cyclin D1 activation [J]. Mol Cell Endocrinol，2014， 382（1）：205-217.
[20] Wan W，Shi Y，Ji L，et al. Interleukin-37 contributes to the pathogenesis of gout by affecting PDZ domain-containing 1 protein through the nuclear factor-kappa B pathway [J]. J Int Med Res，2020，48（9）：300060520948 717.
[21] Zhao C，Tao T，Yang L，et al. Loss of PDZK1 expression activates PI3K/AKT signaling via PTEN phosphorylation in gastric cancer [J]. Cancer Lett，2019，453：107-121.
[22] Kim H，Abd Elmageed ZY，Ju J，et al. PDZK1 is a novel factor in breast cancer that is indirectly regulated by estrogen through IGF-1R and promotes estrogen-mediated growth [J]. Mol Med，2013，19（1）：253-262.
[23] Zheng J，Wang L，Peng Z，et al. Low level of PDZ domain containing 1 （PDZK1） predicts poor clinical outcome in patients with clear cell renal cell carcinoma [J]. EBio Medicine，2017，15：62-72.
[24] Wang N，Zheng Y，Zhang X，et al. Roles of circ_0000135/miR-140-3p/PDZK1 network in cervical cancer [J]. Clin Transl Oncol，2022.
[25] Qi Y，Ma Y，Peng Z，et al. Long noncoding RNA PENG upregulates PDZK1 expression by sponging miR-15b to suppress clear cell renal cell carcinoma cell proliferation [J]. Oncogene，2020，39（22）：4404-4420.
[26] Handa O，Goda K，Handa Y，et al. PDZK1 induces resistance to apoptosis in esophageal adenocarcinoma cells [J]. Esophagus，2021，18（3）：655-662. |
|
|
|
