human thyroid medullary cancer cell line tt  (ATCC)

Journal: iScience

Article Title: AURKB and PI3K/AKT/mTOR pathways converge to regulate TERT expression

doi: 10.1016/j.isci.2025.113194

Figure Lengend Snippet: Identification of kinase inhibitors that repress TERTp MUT reporter activity (A) Schematic diagram of knock-in strategy. LUC : luciferase, PURO : Puromycin, LHA: left homology arm, RHA: right homology arm, HDR: homology directed repair. (B) Quantification of transgene copy number and TERT expression in SW1736 TERT/LUC . Digital droplet PCR and RT-qPCR were utilized to quantify the transgene copy number and TERT expression, respectively, from gDNA and total RNA extracted from SW1736 TERT/LUC across 30 passages post-puromycin selection. The plotted values represent averages from three independent assays. (C) Genome-wide coverage plot derived from Oxford Nanopore long-read sequencing of SW1736 TERT/LUC . An inset zooms in on the TERT locus, where a distinct peak indicates the precise integration site of the LUC transgene at the TERT locus. (D and E) Sanger sequencing analysis of the reporter integration site in PCR amplified genomic DNA from SW1736 TERT/LUC reporter cells. TSS : TERT transcriptional start site, LUC : luciferase gene (E) A library of 218 FDA-approved and experimental inhibitors was tested against the SW1736 TERT/LUC reporter cell-line. The heatmap show hierarchical clustering of mean values of two independent screens performed in duplicate, which were normalized to Actinomycin D (general transcriptional inhibitor) and DMSO controls and expressed as percentages of the DMSO control. The inhibitors within clusters 1 and 2 are shown together with their respective targets. (F) Dose response of SW1736 TERT/LUC cells treated with AZD8330 (target = MEK1/2), AZD8055 (mTORC1/2), Lenvatinib (RTK), Dabrafenib (RAF) and Everolimus (mTORC1). Luciferase activity was evaluated after 24 h treatment with varying inhibitor doses (0.01–20 μM). Plotted values are the mean ± SD of three independent experiments, each performed in triplicate, expressed as fold-change in normalized percentage luciferase activity relative to DMSO treated cells.

Article Snippet: Human SW1736 thyroid cancer cell line , CLS Cell Lines Service GmbH, Eppelheim, Germany , Cat#: 300453 RRID: CVCL_3883.

Techniques: Activity Assay, Knock-In, Luciferase, Expressing, Quantitative RT-PCR, Selection, Genome Wide, Derivative Assay, Sequencing, Amplification, Control

Journal: iScience

Article Title: AURKB and PI3K/AKT/mTOR pathways converge to regulate TERT expression

doi: 10.1016/j.isci.2025.113194

Figure Lengend Snippet: PI3K/AKT/mTOR pathway modulates TERT expression and activity in thyroid cancer (A and B) Correlation between TERT expression and (A) phospho-AKT (S473) and (B) phospho-MAPK (T202/Y204) levels, in TERTp mutated thyroid tumor cell lines: TPC1 (PTC), SW1736, 8505C, and C643 (ATC), alongside the non-malignant NThy-ori-3.1 cell line. TERT expression was quantified using RT-qPCR, and phospho-protein levels were assessed through semi-quantitative western blotting. (C–E) Correlation of Somatic Variants in MAPK and PI3K/AKT/mTOR Pathways with TERT Expression in six poorly differentiated thyroid carcinoma (PDTC) cases. WGS mutational profiling of key thyroid cancer driver and PI3K/AKT/mTOR pathway genes versus log2FC TERT expression, as determined by RT-qPCR, compared to the median expression levels across six cases of PDTC. Colors in the top row indicate whether a somatic variant impacts the MAPK, PI3K/AKT/mTOR or both pathways. Time-course analysis of (D) TERT expression 24–72 h measured by RT-qPCR and (E) telomerase activity relative to MCF7 control 72–120 h measured by qTRAP, following treatment with Everolimus (IC50 dose of 2 nM) across various cancer cell lines. Significant changes (∗), defined as p < 0.05, were calculated by two-tailed unpaired t -test.

Article Snippet: Human SW1736 thyroid cancer cell line , CLS Cell Lines Service GmbH, Eppelheim, Germany , Cat#: 300453 RRID: CVCL_3883.

Techniques: Expressing, Activity Assay, Quantitative RT-PCR, Western Blot, Variant Assay, Control, Two Tailed Test

Journal: iScience

Article Title: AURKB and PI3K/AKT/mTOR pathways converge to regulate TERT expression

doi: 10.1016/j.isci.2025.113194

Figure Lengend Snippet: Correlation and impact of AURKB expression on TERT levels in thyroid cancer subtypes (A) Thyroid cancer cells transfected with AURKB-specific shRNA plasmids were harvested following 4-day puromycin selection for assessment of AURKB levels by western blotting and TERT by RT-qPCR. Plotted values are the mean ± SD of three independent experiments, each performed in triplicate, expressed as fold-change in normalized expression relative to untransfected control. (B–F) Correlation between TERT and AURKB expression determined by RT-qPCR in TERTp mutated thyroid tumor cell lines: TPC1 (PTC), SW1736, 8505C, and C643 (ATC), alongside the non-malignant NThy-ori-3.1 cell line. Correlation between TERT and AURKB expression in (C) 220 PTC samples from the TCGA study, and (D) 37 advanced thyroid cancers from the Landa et al. study, using z-scores calculated from available transcriptomic data. Quantitative ChIP of AURKB, EZH2 and H3S10ph, H3K4Me3 and H3K27Me3 epigenetic marks at specific regions spanning the TERT transcriptional start site. Chromatin was prepared from (E) mutant C643 or TPC1, and (F) wild-type CAL62 and MDAT-T41 cells treated for 24 h with either 180 nM Hesperadin or DMSO. Plotted values are the mean average ± SD of three independent experiments. For all experiments, asterisks (∗) denote significant changes, determined at p < 0.05, using an unpaired two-tailed t -test with the assumption of equal variances.

Article Snippet: Human SW1736 thyroid cancer cell line , CLS Cell Lines Service GmbH, Eppelheim, Germany , Cat#: 300453 RRID: CVCL_3883.

Techniques: Expressing, Transfection, shRNA, Selection, Western Blot, Quantitative RT-PCR, Control, Mutagenesis, Two Tailed Test

Journal: iScience

Article Title: AURKB and PI3K/AKT/mTOR pathways converge to regulate TERT expression

doi: 10.1016/j.isci.2025.113194

Figure Lengend Snippet: Impact of AURKB inhibition on TERT expression and telomerase activity (A–C) Dose response of TERT expression measured by RT-qPCR across thyroid cancer cell-lines treated with 0.1–10 μM Hesperadin. Plotted values are the mean ± SD of three independent experiments, each performed in triplicate, expressed as fold-change in normalized expression relative to DMSO control. Time-course analysis showing modulation of (B) TERT expression 24–72 h measured by RT-qPCR and (C) telomerase activity relative to MCF7 control 72–120 h measured by qTRAP, following treatment with IC50 dose of Hesperadin across various cancer cell lines. (D–F), Cell-cycle independent effect of Hesperadin on TERT expression was assessed by RT-qPCR at 0, 3, and 6 h post IC50 Hesperadin dose in SW1736 and CAL62 cells, which were arrested at the G2/M phase by Nocodazole. Flow cytometry was utilized to evaluate the cell cycle distribution of cells exposed to a 24 h Nocodazole vehicle, 24 h Nocodazole with a 6 h Hesperadin vehicle, or Nocodazole plus 6 h Hesperadin treatment. Data illustrates average cell percentages in G1, S, and G2/M phases (±SD). Values presented are mean ± SD from three independent experiments, each conducted in triplicate, expressed as fold changes in normalized expression/activity relative to 0 h baseline levels. For all experiments, asterisks (∗) denote significant changes, determined at p < 0.05, using an unpaired two-tailed t -test with the assumption of equal variances.

Article Snippet: Human SW1736 thyroid cancer cell line , CLS Cell Lines Service GmbH, Eppelheim, Germany , Cat#: 300453 RRID: CVCL_3883.

Techniques: Inhibition, Expressing, Activity Assay, Quantitative RT-PCR, Control, Flow Cytometry, Two Tailed Test

Journal: iScience

Article Title: AURKB and PI3K/AKT/mTOR pathways converge to regulate TERT expression

doi: 10.1016/j.isci.2025.113194

Figure Lengend Snippet: mTORC1 inhibition leads to the dissociation of TRIM28-TRIM24 and AURKB from the mutant TERT promoter (A–F) Representative western blot images showing TRIM28 and TRIM24 expression across thyroid cell-lines. Co-immunoprecipitation of (B) endogenous TRIM24 in SW1736 and C643 cells; or (C) exogenous flag-tagged proteins overexpressed in SW1736 cells. Whole-cell lysates were incubated with anti-TRIM28 or IgG antibody for IP. (D, Left hand panel) Representative western blot images showing REST and expression across thyroid cell-lines. (D, Right hand panel) Co-immunoprecipitation of endogenous TRIM28 and AURKB by REST proteins in SW1736. Quantitative ChIP analysis was performed to measure TRIM28, TRIM24, AURKB, REST, EZH2 and H3S10ph levels at specific regions around the TERT transcriptional start site in (E) TPC1 and C643, and (F) CAL62 and MDAT-T41 cell following treatment with 2 nM Everolimus or DMSO for 6 h. The plotted values represent the mean ± SD derived from three independent experiments. In all experiments, asterisks (∗) indicate significant changes, determined at p < 0.05 using an unpaired two-tailed t -test with the assumption of equal variances.

Article Snippet: Human SW1736 thyroid cancer cell line , CLS Cell Lines Service GmbH, Eppelheim, Germany , Cat#: 300453 RRID: CVCL_3883.

Techniques: Inhibition, Mutagenesis, Western Blot, Expressing, Immunoprecipitation, Incubation, Derivative Assay, Two Tailed Test

Journal: iScience

Article Title: AURKB and PI3K/AKT/mTOR pathways converge to regulate TERT expression

doi: 10.1016/j.isci.2025.113194

Figure Lengend Snippet: PI3K/AKT/mTOR pathway modulates TERT expression and activity in thyroid cancer (A and B) Correlation between TERT expression and (A) phospho-AKT (S473) and (B) phospho-MAPK (T202/Y204) levels, in TERTp mutated thyroid tumor cell lines: TPC1 (PTC), SW1736, 8505C, and C643 (ATC), alongside the non-malignant NThy-ori-3.1 cell line. TERT expression was quantified using RT-qPCR, and phospho-protein levels were assessed through semi-quantitative western blotting. (C–E) Correlation of Somatic Variants in MAPK and PI3K/AKT/mTOR Pathways with TERT Expression in six poorly differentiated thyroid carcinoma (PDTC) cases. WGS mutational profiling of key thyroid cancer driver and PI3K/AKT/mTOR pathway genes versus log2FC TERT expression, as determined by RT-qPCR, compared to the median expression levels across six cases of PDTC. Colors in the top row indicate whether a somatic variant impacts the MAPK, PI3K/AKT/mTOR or both pathways. Time-course analysis of (D) TERT expression 24–72 h measured by RT-qPCR and (E) telomerase activity relative to MCF7 control 72–120 h measured by qTRAP, following treatment with Everolimus (IC50 dose of 2 nM) across various cancer cell lines. Significant changes (∗), defined as p < 0.05, were calculated by two-tailed unpaired t -test.

Article Snippet: Human C643 thyroid cancer cell line , CLS Cell Lines Service GmbH, Eppelheim, Germany , Cat#: 300298 RRID: CVCL_5969.

Techniques: Expressing, Activity Assay, Quantitative RT-PCR, Western Blot, Variant Assay, Control, Two Tailed Test

Journal: iScience

Article Title: AURKB and PI3K/AKT/mTOR pathways converge to regulate TERT expression

doi: 10.1016/j.isci.2025.113194

Figure Lengend Snippet: Correlation and impact of AURKB expression on TERT levels in thyroid cancer subtypes (A) Thyroid cancer cells transfected with AURKB-specific shRNA plasmids were harvested following 4-day puromycin selection for assessment of AURKB levels by western blotting and TERT by RT-qPCR. Plotted values are the mean ± SD of three independent experiments, each performed in triplicate, expressed as fold-change in normalized expression relative to untransfected control. (B–F) Correlation between TERT and AURKB expression determined by RT-qPCR in TERTp mutated thyroid tumor cell lines: TPC1 (PTC), SW1736, 8505C, and C643 (ATC), alongside the non-malignant NThy-ori-3.1 cell line. Correlation between TERT and AURKB expression in (C) 220 PTC samples from the TCGA study, and (D) 37 advanced thyroid cancers from the Landa et al. study, using z-scores calculated from available transcriptomic data. Quantitative ChIP of AURKB, EZH2 and H3S10ph, H3K4Me3 and H3K27Me3 epigenetic marks at specific regions spanning the TERT transcriptional start site. Chromatin was prepared from (E) mutant C643 or TPC1, and (F) wild-type CAL62 and MDAT-T41 cells treated for 24 h with either 180 nM Hesperadin or DMSO. Plotted values are the mean average ± SD of three independent experiments. For all experiments, asterisks (∗) denote significant changes, determined at p < 0.05, using an unpaired two-tailed t -test with the assumption of equal variances.

Article Snippet: Human C643 thyroid cancer cell line , CLS Cell Lines Service GmbH, Eppelheim, Germany , Cat#: 300298 RRID: CVCL_5969.

Techniques: Expressing, Transfection, shRNA, Selection, Western Blot, Quantitative RT-PCR, Control, Mutagenesis, Two Tailed Test

Journal: iScience

Article Title: AURKB and PI3K/AKT/mTOR pathways converge to regulate TERT expression

doi: 10.1016/j.isci.2025.113194

Figure Lengend Snippet: mTORC1 inhibition leads to the dissociation of TRIM28-TRIM24 and AURKB from the mutant TERT promoter (A–F) Representative western blot images showing TRIM28 and TRIM24 expression across thyroid cell-lines. Co-immunoprecipitation of (B) endogenous TRIM24 in SW1736 and C643 cells; or (C) exogenous flag-tagged proteins overexpressed in SW1736 cells. Whole-cell lysates were incubated with anti-TRIM28 or IgG antibody for IP. (D, Left hand panel) Representative western blot images showing REST and expression across thyroid cell-lines. (D, Right hand panel) Co-immunoprecipitation of endogenous TRIM28 and AURKB by REST proteins in SW1736. Quantitative ChIP analysis was performed to measure TRIM28, TRIM24, AURKB, REST, EZH2 and H3S10ph levels at specific regions around the TERT transcriptional start site in (E) TPC1 and C643, and (F) CAL62 and MDAT-T41 cell following treatment with 2 nM Everolimus or DMSO for 6 h. The plotted values represent the mean ± SD derived from three independent experiments. In all experiments, asterisks (∗) indicate significant changes, determined at p < 0.05 using an unpaired two-tailed t -test with the assumption of equal variances.

Article Snippet: Human C643 thyroid cancer cell line , CLS Cell Lines Service GmbH, Eppelheim, Germany , Cat#: 300298 RRID: CVCL_5969.

Techniques: Inhibition, Mutagenesis, Western Blot, Expressing, Immunoprecipitation, Incubation, Derivative Assay, Two Tailed Test

Journal: bioRxiv

Article Title: CRISPR-Based Gene Dependency Screens reveal Mechanism of BRAF Inhibitor Resistance in Anaplastic Thyroid Cancer

doi: 10.1101/2025.06.26.661609

Figure Lengend Snippet: A. Human focused CRISPR/Cas9 KO library and CRISPR/dcas9 activation library containing number of guides were packed into lentiviral particles and transduced into Cas9+ or dCas9+ 8505c cells. The transduced cells were selected with puromycin. Newly generated mutant cell lines were cultured for 14 days with vehicle or dabrafenib (0.4 µM) for screening. Genomic DNA was extracted from the treated cells with vehicle or dabrafenib, sgRNA fragments were amplified by RT-PCR followed by next-generation sequencing. Genomic DNA from non-treated 8505c-transduced cell line was used as control. Sequencing data were analyzed using MAGeCKFlute. Genes were ranked by essentiality. B . Top 10 hits from the CRISPR/Cas9 KO at 14 days of dabrafenib treatment based on differential beta score . C. Top 50 “essential genes” from CRISPR/dCas9 activation screen. Red arrow pointing to HGF and blue arrow pointing to WWTR1. D . Venn Diagram showing the common essential genes from the CRISPR/Cas9 KO and activation screens’ top 50 hits. E. sgRNA targeting WWTR1 (TAZ) were depleted in dabrafenib treated cells and sgRNA activating WWTR1 were enriched in dabrafenib treated cells, suggesting that WWTR1 is an essential gene for survival during treatment. F . Cancer Dependency Map showing gene effect of WWTR1 using CHRONOS score in thyroid cancer cell lines . G . Gene expression Omnibus dataset (GSE33630) showed higher expression of WWTR1 in ATC compared to normal thyroid or PTC. H . WWTR1 (TAZ) essentiality in cancer cell lines based on BRAF mutation status using DepMap dataset. Essentiality score is defined by the effect of WWTR1 loss on cell viability. BRAFV600E-driven cancer cells are more sensitive to WWTR1 KO (TAZ KO) than non-BRAFV600E cells. *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001

Article Snippet: The human anaplastic thyroid cancer cell line 8505c (Sigmal Millipore) was grown at 37°C with 5% CO 2 in Dulbecco’s Modified Eagle Medium (DMEM) (HyClone) supplemented with 10% Fetal Bovine Serum (Gemini Bio) and 1% Penicillin Streptomycin (Gibco).

Techniques: CRISPR, Activation Assay, Generated, Mutagenesis, Cell Culture, Amplification, Reverse Transcription Polymerase Chain Reaction, Next-Generation Sequencing, Control, Sequencing, Gene Expression, Expressing

Journal: bioRxiv

Article Title: CRISPR-Based Gene Dependency Screens reveal Mechanism of BRAF Inhibitor Resistance in Anaplastic Thyroid Cancer

doi: 10.1101/2025.06.26.661609

Figure Lengend Snippet: A. Depletion of TAZ using shRNA showed a mild effect on cell viability, However, it significantly reduced cell growth in the presence of dabrafenib B . Top and bottom panel, Colony formation assay showing that TAZ depletion sensitizes ATC cells to dabrafenib. C . TAZ-knock out markedly reduces colonies formation upon dabrafenib treatment . D. TAZ expression by western blot and RT PCR in shTAZ cells, and TAZ KO cells using CRISPR/Cas9 system and sgWWTR1-sg1 and sgWWTR1-sg2. E, F . TAZ-TEAD inhibitors, GNE-7933 and K-975 sensitized 8505c to dabrafenib. G . ATC patient-derived spheroids showed a significant reduction of cell viability in cell spheroids treated with the combination of GNE-7933 and dabrafenib compared to single agents. H . Immunoprecipitation assay showed a reduction of the binding of TAZ to TEAD with K-975 and GNE-7933. *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001.

Article Snippet: The human anaplastic thyroid cancer cell line 8505c (Sigmal Millipore) was grown at 37°C with 5% CO 2 in Dulbecco’s Modified Eagle Medium (DMEM) (HyClone) supplemented with 10% Fetal Bovine Serum (Gemini Bio) and 1% Penicillin Streptomycin (Gibco).

Techniques: shRNA, Colony Assay, Knock-Out, Expressing, Western Blot, Reverse Transcription Polymerase Chain Reaction, CRISPR, Derivative Assay, Immunoprecipitation, Binding Assay

Journal: bioRxiv

Article Title: CRISPR-Based Gene Dependency Screens reveal Mechanism of BRAF Inhibitor Resistance in Anaplastic Thyroid Cancer

doi: 10.1101/2025.06.26.661609

Figure Lengend Snippet: A. Tumor growth curves of tumor xenografts in immunocompromised mice. 8505c-shCtrl or 8505c-shTAZ cells were implanted subcutaneously into the flanks. Treatment with vehicle or dabrafenib was initiated 2 weeks after tumor implantation. Dabrafenib was administered daily by gavage. Tumor diameters were measured weekly and used to calculate tumor volume. Data show mean±SEM ( n = 8 or 10). B . Tumor weight was recorded ex vivo. C . Animal weight recorded at the end of the experiment showing no weight loss due to dabrafenib treatment. D . Ex vivo images of the tumors harvested at the end point of the experiment E. Kaplan Meier survival curve after dabrafenib withdrawal. F . Growth curve over time of each tumor implanted for up to 3 weeks post drug withdrawal. *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001

Article Snippet: The human anaplastic thyroid cancer cell line 8505c (Sigmal Millipore) was grown at 37°C with 5% CO 2 in Dulbecco’s Modified Eagle Medium (DMEM) (HyClone) supplemented with 10% Fetal Bovine Serum (Gemini Bio) and 1% Penicillin Streptomycin (Gibco).

Techniques: Tumor Implantation, Ex Vivo

Journal: bioRxiv

Article Title: CRISPR-Based Gene Dependency Screens reveal Mechanism of BRAF Inhibitor Resistance in Anaplastic Thyroid Cancer

doi: 10.1101/2025.06.26.661609

Figure Lengend Snippet: A. CBR-5884 sensitizes 8505c to dabrafenib and B . reduces PHGDH expression. C . GSK2606414 reduces ATF4 expression after 1 hour of treatment and sensitizes 8505c to dabrafenib. D, E . CBR-5884 and GSK2606414 sensitizes patient-derived spheroids (ATC-01) to dabrafenib after 10 days of treatment. *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001.

Article Snippet: The human anaplastic thyroid cancer cell line 8505c (Sigmal Millipore) was grown at 37°C with 5% CO 2 in Dulbecco’s Modified Eagle Medium (DMEM) (HyClone) supplemented with 10% Fetal Bovine Serum (Gemini Bio) and 1% Penicillin Streptomycin (Gibco).

Techniques: Expressing, Derivative Assay

Journal: Annals of Medicine

Article Title: Human adipose-derived stem cells promote migration of papillary thyroid cancer cell via leptin pathway

doi: 10.1080/07853890.2024.2419990

Figure Lengend Snippet: The conditioned medium of ADSCs enhanced the invasion and migration of TPC-1 and BCPAP cells. (A) The supernatant of ADSCs medium was collected and filtered as the conditioned medium. (B) In the transwell assay, the conditioned medium of ADSCs (ADSC-CM) significantly enhanced the invasion of TPC-1/BCPAP cells. (C) In the wound healing assay, ADSC-CM improved the mobility of TPC-1/BCPAP cells. Experiments were repeated at least five times. Data are expressed as mean ± standard deviation. * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: The TPC-1 and BCPAP human papillary thyroid cancer cell lines (Procell Life Science & Technology, Co., Ltd.) were cultured in RPMI-1640 medium (Thermo Fisher Scientific, Inc.) containing 10% fetal bovine serum [ , ].

Techniques: Migration, Transwell Assay, Wound Healing Assay, Standard Deviation

Journal: Annals of Medicine

Article Title: Human adipose-derived stem cells promote migration of papillary thyroid cancer cell via leptin pathway

doi: 10.1080/07853890.2024.2419990

Figure Lengend Snippet: ADSC-CM Improved the proliferation and viability of TPC-1 and BCPAP cells. (A,C) EdU incorporation assay showed that ADSC-CM upregulated the proliferation of TPC-1 and BCPAP. (B,D) CCK8 assay showed that ADSC-CM increased the cell viability of TPC-1 and BCPAP. Experiments were repeated at least five times. Data are expressed as mean ± standard deviation. * p < 0.05, ** p < 0.01.

Article Snippet: The TPC-1 and BCPAP human papillary thyroid cancer cell lines (Procell Life Science & Technology, Co., Ltd.) were cultured in RPMI-1640 medium (Thermo Fisher Scientific, Inc.) containing 10% fetal bovine serum [ , ].

Techniques: CCK-8 Assay, Standard Deviation

Journal: Annals of Medicine

Article Title: Human adipose-derived stem cells promote migration of papillary thyroid cancer cell via leptin pathway

doi: 10.1080/07853890.2024.2419990

Figure Lengend Snippet: The conditioned medium of ADSCs upregulated the level of leptin receptor (Ob-R) in TPC-1 and BCPAP cells. (A) The concentration of leptin in the medium of ADSCs was ∼3-fold higher than that in the medium of TPC-1 and BCPAP cells, approximately 50 pg/ml. (B) In vitro experiments showed that ADSC-CM increased the level of leptin receptor (Ob-R) in the TPC-1/BCPAP cells. Experiments were repeated at least five times. Data are expressed as mean ± standard deviation. * p < 0.05, *** p < 0.001.

Article Snippet: The TPC-1 and BCPAP human papillary thyroid cancer cell lines (Procell Life Science & Technology, Co., Ltd.) were cultured in RPMI-1640 medium (Thermo Fisher Scientific, Inc.) containing 10% fetal bovine serum [ , ].

Techniques: Concentration Assay, In Vitro, Standard Deviation

Journal: Annals of Medicine

Article Title: Human adipose-derived stem cells promote migration of papillary thyroid cancer cell via leptin pathway

doi: 10.1080/07853890.2024.2419990

Figure Lengend Snippet: The neutralizing antibody to leptin reduced the invasion and migration of the TPC-1 and BCPAP cells. ADSC-CM upregulated MMP-2 in TPC-1 and BCPAP cells, and the effect was attenuated by the neutralizing antibody to leptin. (A) Addition of 10 μg/mL NAB of leptin to ADSC-CM conditioned medium attenuated TPC-1 and BCPAP invasion. (B) Leptin NAB also attenuated conditioned medium-promoted TPC-1/BCPAP migration. Experiments were repeated at least five times. Data are expressed as mean ± standard deviation. * p < 0.05, *** p < 0.001.

Article Snippet: The TPC-1 and BCPAP human papillary thyroid cancer cell lines (Procell Life Science & Technology, Co., Ltd.) were cultured in RPMI-1640 medium (Thermo Fisher Scientific, Inc.) containing 10% fetal bovine serum [ , ].

Techniques: Migration, Standard Deviation

Journal: Annals of Medicine

Article Title: Human adipose-derived stem cells promote migration of papillary thyroid cancer cell via leptin pathway

doi: 10.1080/07853890.2024.2419990

Figure Lengend Snippet: Neutralizing antibodies against leptin slightly downregulated cell proliferation without significant effect on cell viability. (A) Addition of leptin NAB to ADSC-CM slightly reduced the stimulatory effect of conditioned medium on TPC-1 proliferation. (B) Addition of NAB to the conditioned medium had no significant effect on cell viability of TPC-1 cells. (C) NAB of leptin had no significant effect on BCPAP proliferation. (D) NAB of leptin had no significant effect on BCPAP viability. Experiments were repeated at least five times. Data are expressed as mean ± standard deviation. * p < 0.05, ns: not statistically significant.

Article Snippet: The TPC-1 and BCPAP human papillary thyroid cancer cell lines (Procell Life Science & Technology, Co., Ltd.) were cultured in RPMI-1640 medium (Thermo Fisher Scientific, Inc.) containing 10% fetal bovine serum [ , ].

Techniques: Standard Deviation

Journal: Annals of Medicine

Article Title: Human adipose-derived stem cells promote migration of papillary thyroid cancer cell via leptin pathway

doi: 10.1080/07853890.2024.2419990

Figure Lengend Snippet: (A,B) The ADSCs conditioned medium upregulated the MMP-2 levels of TPC-1/BCPAP. NAB of leptin partially counteracted the increase in MMP-2 levels. Experiments were repeated at least five times. Data are expressed as mean ± standard deviation. * p < 0.05, ** p < 0.01.

Article Snippet: The TPC-1 and BCPAP human papillary thyroid cancer cell lines (Procell Life Science & Technology, Co., Ltd.) were cultured in RPMI-1640 medium (Thermo Fisher Scientific, Inc.) containing 10% fetal bovine serum [ , ].

Techniques: Standard Deviation