中华核医学杂志
中華覈醫學雜誌
중화핵의학잡지
CHINESE JOURNAL OF NUCLEAR MEDICINE
2010年
2期
116-119
,共4页
包建东%林秀峰%俞惠新%谭成%张莉
包建東%林秀峰%俞惠新%譚成%張莉
포건동%림수봉%유혜신%담성%장리
甲状腺肿瘤%钠/碘转运体%基因表达%碘%组蛋白脱乙酰基酶%酶抑制剂
甲狀腺腫瘤%鈉/碘轉運體%基因錶達%碘%組蛋白脫乙酰基酶%酶抑製劑
갑상선종류%납/전전운체%기인표체%전%조단백탈을선기매%매억제제
Throid neoplasms%Sodium-iodide symporter%Gene expression%Iodine%Histone deacetylase%Enzyme imhibitors
目的 探讨曲古菌素A(TSA)对甲状腺癌细胞中钠/碘同向转运蛋白(NTIS)基因表达和摄取碘的影响.方法 以不同浓度的TSA诱导滤泡状甲状腺癌细胞FTC-133及乳头状甲状腺癌细胞KI,利用反转录-聚合酶链反应(RT-PCR)分析经诱导后2株甲状腺癌细胞中NIS mRNA的表达,以NIS/3-磷酸甘油醛脱氧酶(GAPDH)的条带密度比值作为mRNA表达强度,并检测诱导前后甲状腺癌细胞对放射性碘摄取的变化.2组数据间比较采用独立样本t检验,多组数据间比较用One-wayANONA方差分析.结果 20,50,75,100和150 nmol/L TSA诱导48 h后.甲状腺癌细胞FTC-133的NIS mRNA表达较未诱导对照组增加了1.5至13.7倍,各TSA浓度组间FTC-133 NIS mRNA表达差异有统计学意义(F=32.56,P<0.01);而K1的NIS mRNA表达没有明显变化,TSA浓度为50和75 nmol/L时表达有所增加(NIS/GAPDH条带密度比值分别为0.62±0.16,0.60±0.23),但与对照组(0.41±0.18)比较差异无统计学意义(F=2.823,P>0.05).细胞摄取碘实验显示,50和75 nmol/L TSA诱导48 h后,FTC-133的摄碘增加[(15.42±0.42)×10~3和(18.98±1.33)×10~3计数·min~(-1)/10~5个细胞],与对照组[(8.46±0.84)×10~3计数·min~(-1)/10~5个细胞]比较,差异有统计学意义(t值分别为3.018和3.557,P均<0.05);而50和75 nmol/L TSA作用后K1对碘的摄取也有增加[(5.83±1.09)×10~3和(6.97±0.65)×10~3计数·min~(-1)/10~5个细胞],但与对照组[(5.37±0.88)×10~3计数·min~(-1)/10~5个细胞]比较,差异无统计学意义(t值分别为0.185和0.332,P均>0.05).结论 TSA能明显诱导滤泡状甲状腺癌细胞的NIS mRNA表达升高和摄碘增加,而对乳头状甲状腺癌细胞作用不明显.
目的 探討麯古菌素A(TSA)對甲狀腺癌細胞中鈉/碘同嚮轉運蛋白(NTIS)基因錶達和攝取碘的影響.方法 以不同濃度的TSA誘導濾泡狀甲狀腺癌細胞FTC-133及乳頭狀甲狀腺癌細胞KI,利用反轉錄-聚閤酶鏈反應(RT-PCR)分析經誘導後2株甲狀腺癌細胞中NIS mRNA的錶達,以NIS/3-燐痠甘油醛脫氧酶(GAPDH)的條帶密度比值作為mRNA錶達彊度,併檢測誘導前後甲狀腺癌細胞對放射性碘攝取的變化.2組數據間比較採用獨立樣本t檢驗,多組數據間比較用One-wayANONA方差分析.結果 20,50,75,100和150 nmol/L TSA誘導48 h後.甲狀腺癌細胞FTC-133的NIS mRNA錶達較未誘導對照組增加瞭1.5至13.7倍,各TSA濃度組間FTC-133 NIS mRNA錶達差異有統計學意義(F=32.56,P<0.01);而K1的NIS mRNA錶達沒有明顯變化,TSA濃度為50和75 nmol/L時錶達有所增加(NIS/GAPDH條帶密度比值分彆為0.62±0.16,0.60±0.23),但與對照組(0.41±0.18)比較差異無統計學意義(F=2.823,P>0.05).細胞攝取碘實驗顯示,50和75 nmol/L TSA誘導48 h後,FTC-133的攝碘增加[(15.42±0.42)×10~3和(18.98±1.33)×10~3計數·min~(-1)/10~5箇細胞],與對照組[(8.46±0.84)×10~3計數·min~(-1)/10~5箇細胞]比較,差異有統計學意義(t值分彆為3.018和3.557,P均<0.05);而50和75 nmol/L TSA作用後K1對碘的攝取也有增加[(5.83±1.09)×10~3和(6.97±0.65)×10~3計數·min~(-1)/10~5箇細胞],但與對照組[(5.37±0.88)×10~3計數·min~(-1)/10~5箇細胞]比較,差異無統計學意義(t值分彆為0.185和0.332,P均>0.05).結論 TSA能明顯誘導濾泡狀甲狀腺癌細胞的NIS mRNA錶達升高和攝碘增加,而對乳頭狀甲狀腺癌細胞作用不明顯.
목적 탐토곡고균소A(TSA)대갑상선암세포중납/전동향전운단백(NTIS)기인표체화섭취전적영향.방법 이불동농도적TSA유도려포상갑상선암세포FTC-133급유두상갑상선암세포KI,이용반전록-취합매련반응(RT-PCR)분석경유도후2주갑상선암세포중NIS mRNA적표체,이NIS/3-린산감유철탈양매(GAPDH)적조대밀도비치작위mRNA표체강도,병검측유도전후갑상선암세포대방사성전섭취적변화.2조수거간비교채용독립양본t검험,다조수거간비교용One-wayANONA방차분석.결과 20,50,75,100화150 nmol/L TSA유도48 h후.갑상선암세포FTC-133적NIS mRNA표체교미유도대조조증가료1.5지13.7배,각TSA농도조간FTC-133 NIS mRNA표체차이유통계학의의(F=32.56,P<0.01);이K1적NIS mRNA표체몰유명현변화,TSA농도위50화75 nmol/L시표체유소증가(NIS/GAPDH조대밀도비치분별위0.62±0.16,0.60±0.23),단여대조조(0.41±0.18)비교차이무통계학의의(F=2.823,P>0.05).세포섭취전실험현시,50화75 nmol/L TSA유도48 h후,FTC-133적섭전증가[(15.42±0.42)×10~3화(18.98±1.33)×10~3계수·min~(-1)/10~5개세포],여대조조[(8.46±0.84)×10~3계수·min~(-1)/10~5개세포]비교,차이유통계학의의(t치분별위3.018화3.557,P균<0.05);이50화75 nmol/L TSA작용후K1대전적섭취야유증가[(5.83±1.09)×10~3화(6.97±0.65)×10~3계수·min~(-1)/10~5개세포],단여대조조[(5.37±0.88)×10~3계수·min~(-1)/10~5개세포]비교,차이무통계학의의(t치분별위0.185화0.332,P균>0.05).결론 TSA능명현유도려포상갑상선암세포적NIS mRNA표체승고화섭전증가,이대유두상갑상선암세포작용불명현.
Objective To investigate the sodium/iodide symporter (NIS) expression and iodide uptake in thyroid cancer cells induced by the histone deacetyltransferase inhibitors (HDACi), Trichostatin A (TSA). Methods Both the thyroid cancer cell lines, follicular thyroid carcinoma cell line FTC-133 and papillary thyroid carcinoma cell line K1, were firstly induced with TSA for 48 h. Then, the expression of NIS mRNA was analysed with reverse transcription-polymerase chain reaction (RT-PCR), the densitometric ratio of NIS/glyceraldehyde 3-phosphate dehydrogenase (GAPDH) was calculated, and the iodide uptake in the thyroid cancer cells was also measured. Independent-sample t-test and one-way analysis of variance (ANOVA) were used to analyze the data. Results For FTC-133 cells, increased NIS mRNA expression was detected after 48 h of TSA treatment, and the changes were dose-dependent (F=32.56, P<0.01).No obvious increasing expression of NIS mRNA was observed in K1 cells after 48 h of TSA treatment (F=2.823, P >0.05). Furthermore, FTC-133 cells showed the ability of accumulating radioiodide with 50 and 75 nmol/L TSA induction for 48 h: (15.42±0.42)×10~3 counts·min~(-1)·10~(-5) cells vs (8.46±0.84)× 10~3 counts·min~(-1)·10~(-5) cells, t=3.018, P<0.05; (18.98±1.33)×10~3 counts·min~(-1)·10~(-5) cells vs (8.46±0.84)×10~3 counts·min~(-1)·10~(-5) cells, t=3.557, P<0.05, respectively, while radioiodide uptake in K1 displayed no significant change after TSA induction: (5.83±1.09)×10~3 counts·min~(-1)·10~(-5) cells, (6.97±0.65)×10~3 counts·min~(-1)·10~(-5) cells vs (5.37±0.88)×10~3 counts·min~(-1)·10~(-5) cells, t=0.185, P> 0.05 and t = 0.332, P > 0.05, respectively. Conclusion TSA induced upregulated NIS mRNA expression in follicular thyroid cancer cells and augmented radioiodide uptake in thyroid cancer cells, while TSA had no remarkable effect on papillary thyroid carcinoma cell.
