PMID- 27748844 OWN - NLM STAT- MEDLINE DCOM- 20170317 LR - 20170317 IS - 1791-2431 (Electronic) IS - 1021-335X (Linking) VI - 36 IP - 6 DP - 2016 Dec TI - Differential glycolytic profile and Warburg effect in papillary thyroid carcinoma cell lines. PG - 3673-3681 LID - 10.3892/or.2016.5142 [doi] AB - Acceleration of glycolysis is a characteristic of neoplasia. Previous studies have shown that a metabolic shift occurs in many tumors and correlates with a negative prognosis. The present study aimed to investigate the glycolytic profile of thyroid carcinoma cell lines. We investigated glycolytic and oxidative parameters of two thyroid carcinoma papillary cell lines (BCPAP and TPC1) and the non-tumor cell line NTHY-ori. All carcinoma cell lines showed higher rates of glycolysis efficiency, when compared to NTHY-ori, as assessed by a higher rate of glucose consumption and lactate production. The BCPAP cell line presented higher rates of growth, as well as elevated intracellular ATP levels, compared to the TPC1 and NTHY-ori cells. We found that glycolysis and activities of pentose phosphate pathway (PPP) regulatory enzymes were significantly different among the carcinoma cell lines, particularly in the mitochondrial hexokinase (HK) activity which was higher in the BCPAP cells than that in the TPC1 cell line which showed a balanced distribution of HK activity between cytoplasmic and mitochondrial subcellular localizations. However, TPC1 had higher levels of glucose‑6-phosphate dehydrogenase activity, suggesting that the PPP is elevated in this cell type. Using high resolution respirometry, we observed that the Warburg effect was present in the BCPAP and TPC1 cells, characterized by low oxygen consumption and high reactive oxygen species production. Overall, these results indicate that both thyroid papillary carcinoma cell lines showed a glycolytic profile. Of note, BCPAP cells presented some relevant differences in cell metabolism compared to TPC1 cells, mainly related to higher mitochondrial-associated HK activity. FAU - Coelho, Raquel Guimaraes AU - Coelho RG AD - Laboratory of Endocrine Physiology, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Rio de Janeiro 21941-902, Brazil. FAU - Cazarin, Juliana de Menezes AU - Cazarin JM AD - Laboratory of Endocrine Physiology, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Rio de Janeiro 21941-902, Brazil. FAU - Cavalcanti de Albuquerque, Joao Paulo Albuquerque AU - Cavalcanti de Albuquerque JP AD - Laboratory of Endocrine Physiology, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Rio de Janeiro 21941-902, Brazil. FAU - de Andrade, Bruno Moulin AU - de Andrade BM AD - Laboratory of Endocrine Physiology, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Rio de Janeiro 21941-902, Brazil. FAU - Carvalho, Denise P AU - Carvalho DP AD - Laboratory of Endocrine Physiology, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Rio de Janeiro 21941-902, Brazil. LA - eng PT - Comparative Study PT - Journal Article DEP - 20161004 PL - Greece TA - Oncol Rep JT - Oncology reports JID - 9422756 RN - 8L70Q75FXE (Adenosine Triphosphate) RN - EC 2.7.1.1 (Hexokinase) SB - IM MH - Adenosine Triphosphate/biosynthesis MH - Carcinoma, Papillary/*metabolism MH - Cell Line, Tumor MH - Cell Proliferation MH - *Glycolysis MH - Hexokinase/metabolism MH - Humans MH - Mitochondria/metabolism MH - Oxidation-Reduction MH - Oxygen Consumption MH - Thyroid Neoplasms/*metabolism EDAT- 2016/10/18 06:00 MHDA- 2017/03/18 06:00 CRDT- 2016/10/18 06:00 PHST- 2016/04/13 00:00 [received] PHST- 2016/06/09 00:00 [accepted] PHST- 2016/10/18 06:00 [pubmed] PHST- 2017/03/18 06:00 [medline] PHST- 2016/10/18 06:00 [entrez] AID - 10.3892/or.2016.5142 [doi] PST - ppublish SO - Oncol Rep. 2016 Dec;36(6):3673-3681. doi: 10.3892/or.2016.5142. Epub 2016 Oct 4.