广东医学2020 年 7 月第 41 卷第14 期Guangdong Medical Journal Jul. 2020, Vol. 41, No. 141421 •HAX—1对口腔鱗状细胞癌细胞的;1：曾殖和
侵袭能力的作用
孙建礼，朱青青，刘飞，赵果
郑州大学第一附属医院、河南省口腔医院口腔外科（河南郑州450000)
【摘要】目的探讨H A X-1对口腔鱗状细胞癌（0S C C)细胞的增殖和侵袭能力的影响及分子机制
方法转染H A X - 1 s i K N A到口 0S C C细胞T S C C A和T c.a8223，抑制H A X- 1表达；构建过表达载体pcUNA.
3. 1 -c-M y c，转染到 T S C C A和Tca8223，过表达c-M yc;A K T激动剂 SC79(0、1、1.5 和2 ixg/mL)分别孵育干
扰了 H A X- 1的 0S C C细胞24 h，免疫印迹（Western blot)检测 0S C C细胞H A X- 1、p-A K T和c - myc 的蛋
白表达量；溴脱氧尿苷（BrdU)方法检测转染后0S C C细胞的增殖能力；M T T方法检测0S C C细胞转染后的活
力；transwe丨丨侵袭实验检测转染后0S C C细胞的侵袭能力■结果0S C C组织中H A X - 1蛋白表达量显著升
高；H A X- 1 siRNA 转染 T S C C A和T('a8223，H A X - 1、p - A K T和 c -niyc•蛋白表达量明显降低；同时，T S C C A
和Tca8223的细胞活力、增殖和侵袭能力均显著被抑制；S C79(1.5和2 jig/niL)孵育干扰了H A X _丨的TSC-
C A和TVa8223，A K T磷酸化水平和c - m y c表达量明显增加.另外，转染poDNA. 3_ 1 - c - M y c到干扰了 H A X-
I的T S C C A和T ca8223,c-m y c蛋白表达量升高，细胞活力、增殖和侵袭能力升高，结论H A X - 1可通过
A K T调节r-m y(‘的表达，进而调控0S C C细胞的增殖和侵袭的能力，为0S C C的防治提供一定的参考价值和
理论基础。
【关键词】口腔鱗状细胞癌；H A X- 1; AKT; c - Myc.
【中图分类号】R739.85;R34 【文献标志码】A
DOI：10. 13820/j. rnki. gdyx. 20193885
Effects of H A X-1on proliferation and invasion of oral squamous cell carcinoma cells. SUN Jian - l i, ZHU
Qing - qing, LIU Fei, ZHAO Guo. Department oj oral surgery, Henan Stomatological Hospital, Zhengzhou450000,
proliferationHenan，China
【Abstract】Objective To investigate the effects of HAX -1on the proliferation and invasion of oral squamous
cell carcinoma (O S C C) cells and its molecular mechanism. Methods HAX —1siRNA was transfected into OSCC cells
TSCCA and Tca8223 to inhibit HAX — 1expression. The overexpression vector pcDNA. 3. 1— c —Myc was constructed and transfected into TSCCA and Tca8223 to overexpress c - Myc. AKT agonist SC79 (0, 1, 1.5 and 2 (xg/mL) was incubated
with OSCC cells that interfered with HAX -1for 24h. The protein expression levels of HAX -1, p - AKT and c - myc in
OSCC cells were assessed by W estern blot. The proliferation of OSCC cells after transfection was assessed using Bromode- oxyuridine ( BrdU) method. The viability of OSCC cells after transfection was tested by MTT assay. The invasion ability of
OSCC cells after transfection was measured l)y trails - well invasion assay. Results The protein expression level of HAX -
1in OSCC tissues was significantly increased. The protein expression levels of HAX -1, p — AKT and c - myc were sig­
nificantly reduced after the transfection of HAX -1siRNA in TSCCA and Tca8223. At the same lim e, the cell viability, proliferation and invasion abilities of TSCCA and Tc*a8223 were significantly inhibited. AKT phosphorviation level and c -
myc expression were significantly increased following the incubation of SC79 (1.5and 2 jjig/rnL) anti HAX -1interfer­
ence in TSCCA and T ca8223, indic ating that the activation of AKT could effectively block tlie effect of HAX -1on c -
myc expression. In addition, transfection of pcDNA. 3. I- c -Myc into TSCCA and Tc*a8223 with HAX -1interference incTeased c — myc protein expression, cell viability, proliferation and invasion abilities. Conclusion HAX — 1can regu­
late the expression of c - myc through AKT, thereby regulating the proliferation and invasion of OSCC cells, providing a
certain reference value and theoretical basis for the prevention and treatment of OSCC.
【Key words】oral squamous cell carcinoma；HAX - 1；AKT；c - M yc
口腔鱗状细胞癌（o r a l squamous c e l l carcinoma, O S C C)又称口腔鱗癌，是常见的口腔黏膜恶性肿瘤，具有局部浸润、高复发及高转移的特性，常伴有颈部 的淋巴转移:1_2]。口腔鳞癌发病机制复杂，目前仍没有特定的分子耙向药物应用于临床[3:。造血基 质_ 1相关蛋白\-1(吧1-3330士16(1卩1'〇
1?丨丨1\-1，1仏-1)首次被发现于丨997年，1^\-1是一种抗凋亡蛋白，导致某些疾病的发生，同时其在肿瘤细

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