天津医药
天津醫藥
천진의약
TIANJIN MEDICAL JOURNAL
2013年
11期
1055-1058
,共4页
宫颈肿瘤%宫颈上皮内瘤样病变%蛋白激酶类%eIF-2激酶%磷酰化%NF-κB
宮頸腫瘤%宮頸上皮內瘤樣病變%蛋白激酶類%eIF-2激酶%燐酰化%NF-κB
궁경종류%궁경상피내류양병변%단백격매류%eIF-2격매%린선화%NF-κB
uterine cervical neoplasms%cervical intraepithelial neoplasia%protein kinases%eIF-2 kinase%phosphory-lation%NF-kappa B
目的：探讨宫颈病变组织内蛋白激酶R（PKR）、核因子（NF）-κB p65的表达及磷酸化的意义，高危型人乳头状瘤病毒（hsHPV）对两者表达及磷酸化的影响，以及三者的关系。方法以67例宫颈癌、149例宫颈上皮内瘤样病变（CINⅠ~Ⅲ）、15例正常人宫颈组织为观察对象。检测各组hsHPV阳性表达情况，采用免疫组化SP法检测组织内PKR、磷酸化型PKR（p-PKR）、NF-κB p65和磷酸化型NF-κB p65（p-NF-κB p65）在上述分组中的表达。结果231例中hsHPV阳性136例，阴性95例。胞浆中PKR、p-PKR在hsHPV阳性组的表达低于hsHPV阴性组（27.2%和11.0%vs 41.1%和21.1%，χ2分别为4.858、4.371，均P＜0.05），在胞浆和胞核中NF-κB p65、p-NF-κB p65在hsHPV阳性组的表达高于hsHPV阴性组（46.3%、25.7%、22.8%和12.5%vs 32.6%、14.7%、11.6%和4.2%，χ2分别为4.345、4.048、4.729、4.650，均P＜0.05）；在胞浆和胞核中NF-κB p65（+）组PKR的阳性表达率低于NF-κB p65（-）组（25.5%vs 38.0%和20.4%vs 36.3%，χ2分别为3.898、4.396，P＜0.05），p-NF-κB p65（+）组在胞浆中PKR的阳性表达率低于p-NF-κB p65（-）组（19.0%vs 36.0%，χ2=4.462，P＜0.05）。结论 hsHPV可能抑制PKR的表达及磷酸化而促进NF-κB p65的表达及磷酸化，NF-κB p65的表达及磷酸化对PKR的表达可能有抑制作用；三者间的调节作用可能与宫颈癌的发生发展有关。
目的：探討宮頸病變組織內蛋白激酶R（PKR）、覈因子（NF）-κB p65的錶達及燐痠化的意義，高危型人乳頭狀瘤病毒（hsHPV）對兩者錶達及燐痠化的影響，以及三者的關繫。方法以67例宮頸癌、149例宮頸上皮內瘤樣病變（CINⅠ~Ⅲ）、15例正常人宮頸組織為觀察對象。檢測各組hsHPV暘性錶達情況，採用免疫組化SP法檢測組織內PKR、燐痠化型PKR（p-PKR）、NF-κB p65和燐痠化型NF-κB p65（p-NF-κB p65）在上述分組中的錶達。結果231例中hsHPV暘性136例，陰性95例。胞漿中PKR、p-PKR在hsHPV暘性組的錶達低于hsHPV陰性組（27.2%和11.0%vs 41.1%和21.1%，χ2分彆為4.858、4.371，均P＜0.05），在胞漿和胞覈中NF-κB p65、p-NF-κB p65在hsHPV暘性組的錶達高于hsHPV陰性組（46.3%、25.7%、22.8%和12.5%vs 32.6%、14.7%、11.6%和4.2%，χ2分彆為4.345、4.048、4.729、4.650，均P＜0.05）；在胞漿和胞覈中NF-κB p65（+）組PKR的暘性錶達率低于NF-κB p65（-）組（25.5%vs 38.0%和20.4%vs 36.3%，χ2分彆為3.898、4.396，P＜0.05），p-NF-κB p65（+）組在胞漿中PKR的暘性錶達率低于p-NF-κB p65（-）組（19.0%vs 36.0%，χ2=4.462，P＜0.05）。結論 hsHPV可能抑製PKR的錶達及燐痠化而促進NF-κB p65的錶達及燐痠化，NF-κB p65的錶達及燐痠化對PKR的錶達可能有抑製作用；三者間的調節作用可能與宮頸癌的髮生髮展有關。
목적：탐토궁경병변조직내단백격매R（PKR）、핵인자（NF）-κB p65적표체급린산화적의의，고위형인유두상류병독（hsHPV）대량자표체급린산화적영향，이급삼자적관계。방법이67례궁경암、149례궁경상피내류양병변（CINⅠ~Ⅲ）、15례정상인궁경조직위관찰대상。검측각조hsHPV양성표체정황，채용면역조화SP법검측조직내PKR、린산화형PKR（p-PKR）、NF-κB p65화린산화형NF-κB p65（p-NF-κB p65）재상술분조중적표체。결과231례중hsHPV양성136례，음성95례。포장중PKR、p-PKR재hsHPV양성조적표체저우hsHPV음성조（27.2%화11.0%vs 41.1%화21.1%，χ2분별위4.858、4.371，균P＜0.05），재포장화포핵중NF-κB p65、p-NF-κB p65재hsHPV양성조적표체고우hsHPV음성조（46.3%、25.7%、22.8%화12.5%vs 32.6%、14.7%、11.6%화4.2%，χ2분별위4.345、4.048、4.729、4.650，균P＜0.05）；재포장화포핵중NF-κB p65（+）조PKR적양성표체솔저우NF-κB p65（-）조（25.5%vs 38.0%화20.4%vs 36.3%，χ2분별위3.898、4.396，P＜0.05），p-NF-κB p65（+）조재포장중PKR적양성표체솔저우p-NF-κB p65（-）조（19.0%vs 36.0%，χ2=4.462，P＜0.05）。결론 hsHPV가능억제PKR적표체급린산화이촉진NF-κB p65적표체급린산화，NF-κB p65적표체급린산화대PKR적표체가능유억제작용；삼자간적조절작용가능여궁경암적발생발전유관。
Objective To identify the significance of expression and phosphorylation of protein kinase R(PKR) and nuclear factor NF-κB p65 in cervical lesions, and the effect of high-risk human papilloma virus(hsHPV) on expression and phosphorylation of R(PKR) and NF-κB p65. Methods A total of 67 patients with cervical cancer, 149 patients with cervi-cal intraepithelial neoplasia (CINⅠ-Ⅲ) and 15 normal control were included in this study. The expression levels of PKR, phosphorylated PKR (p-PKR), NF-κB p65 and phosphorylated NF-κB p65 (p-NF-κB p65) were detected by immunohisto-chemical SP method in three groups. Results The positive expression rates of PKR and p-PKR in cytoplasm were signifi-cantly lower in hsHPV positive group than those in hsHPV negative group (27.2% and 11.0% vs 41.1% and 21.1%,χ2 =4.858 and 4.371,P<0.05). The positive expression rates of NF-κB p65 and p-NF-κB p65 in cytoplasm and nucleus were significantly higher in hsHPV positive group than those in hsHPV negative group (46.3%, 25.7%, 22.8% and 12.5% vs 32.6%, 14.7%, 11.6%and 4.2%,χ2=4.345,4.048,4.729 and 4.650 respectively,P<0.05). The positive expression rates of PKR in kytoplasm and karyon were significantly lower in NF-κB p65 (+) group than those in NF-κB p65 (-) group (25.5%vs 38.0%and 20.4%vs 36.3%,χ2=3.898 and 4.396 respectively, P<0.05). The positive expression rate of PKR in kyto-plasm was significantly lower in p-NF-κB p65 (+) group than those in p-NF-κB p65 (-) group (19.0%vs 36.0%,χ2=4.462, P<0.05). Conclusion hsHPV may inhibit the expression and phosphorylation of PKR but promote the expression and phosphorylation of NF-κB p65. The expression and phosphorylation of NF-κB p65 may inhibit the expression of PKR. Regu-lating effects of three may be associated with the generation and progression of cervical cancer.
