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[摘要] 目的 探討HOX转录反义RNA（HOTAIR）和微小RNA（miR）-613在食管鳞癌细胞中的调控关系及其对细胞增殖与细胞凋亡的影响。
方法 采用实时荧光定量聚合酶链反应（RT-qPCR）检测食管鳞癌细胞中HOTAIR和miR-613的表达情况，双荧光素酶报告基因实验检测HOTAIR和miR-613靶向关系，CCK-8法和流式细胞仪检测细胞增殖和凋亡。
结果 与其他食管鳞癌细胞相比，人食管鳞癌细胞株Eca-109细胞中HOTAIR表达最高而且miR-613表达水平最低（F=48.56、56.28，P<0.05）。HOTAIR可靶向调控miR-613的表达。下调HOTAIR的表达明显抑制了Eca-109细胞增殖，提高了细胞凋亡和miR-613表达水平（F=205.28～396.53，P<0.05）;抑制miR-613表达后，Eca-109细胞增殖能力明显增强，而细胞凋亡能力明显减弱（F=51.04、511.37，P<0.05）。
结论 下调HOTAIR可通过调控miR-613表达抑制食管鳞癌Eca-109细胞增殖并促进其凋亡。
[关键词] 食管鳞状细胞癌;HOX转录反义RNA;RNA，长链非编码;微RNAs;细胞增殖;细胞凋亡
[中图分类号] R735.1;R342.2
[文献标志码] A
[文章编号] 2096-5532（2021）05-0736-06
doi：10.11712/jms.2096-5532.2021.57.171
[开放科学（资源服务）标识码（OSID）]
[网络出版] https：//kns.cnki.net/kcms/detail/37.1517.r.20211029.1732.002.html;2021-11-02 13：27：02
EFFECT OF THE EXPRESSION OF HOX TRANSCRIPT ANTISENSE INTERGENIC RNA AND MICRORNA-613 ON THE PROLIFERATION AND APOPTOSIS OF ESOPHAGEAL SQUAMOUS CELL CARCINOMA CELLS
CHEN Zhijun， CAO Ke-
xin， ZHU Deqi， GAN Shaoyin， WANG Zhongmin
（Department of Thoracic Surgery， The First Affiliated Hospital of Xinxiang Medical University， Xinxiang 453100， China）
[ABSTRACT] Objective To investigate the regulatory role of HOX transcript antisense intergenic RNA （HOTAIR） and microRNA-613 （miR-613） in esophageal squamous cell carcinoma cells and their effect on cell proliferation and apoptosis.
Me-
thods Quantitative real-time PCR was used to measure the expression of HOTAIR and miR-613 in esophageal squamous cell carcinoma cells; dual luciferase reporter gene assay was used to detect the targeting relationship between HOTAIR and miR-613; CCK-8 assay and flow cytometry were used to measure cell proliferation and apoptosis.
Results Compared with other esophageal squamous cell carcinoma cell lines， the human esophageal squamous cell carcinoma cell line Eca-109 had the highest expression level of HOTAIR and the lowest expression level of miR-613 （F=48.56，56.28;P<0.05）. HOTAIR showed targeted regulation of miR-613 expression. Downregulation of HOTAIR expression significantly inhibited the proliferation of Eca-109 cells and increased cell apoptosis and the expression level of miR-613 （F=205.28-396.53，P<0.05）. After the expression of miR-613 was inhibited， Eca-109 cells showed a significant increase in proliferation and a significant reduction in apoptosis （F=51.04，511.37;P<0.05）. [10]KANG M， LI Y， ZHU S T， et al. MicroRNA-193b Acts as a tumor suppressor gene in human esophageal squamous cell carcinoma via target regulation of KRAS[J]. Oncology Letters， 2019，17（4）：3965-3973.
[11]刘灿，陈丹杰，余军林，等. 晚期食管鳞癌患者血清sPD-L1与组织PD-L1的表达及与预后的关系[J]. 郑州大学学报（医学版）， 2019，54（4）：500-503.
[12]张常，王新文，王亮，等. “垃圾”DNA的奥秘[J]. 科学通报， 2016，61（Z2）：3079-3084.
[13]ZHANG R， XIA L Q， LU W W， et al. LncRNAs and cancer[J]. Oncology Letters， 2016，12（2）：1233-1239.
[14]REDDY K B. MicroRNA （miRNA） in cancer[J]. Cancer Cell International， 2015，15：38.
[15]ZHAO W Y， GENG D H， LI S Q， et al. LncRNA HOTAIR influences cell growth， migration， invasion， and apoptosis via the miR-20a-5p/HMGA2 axis in breast cancer[J]. Cancer Medicine， 2018，7（3）：842-855.
[16]LIU M Z， JIA J Y， WANG X J， et al. Long non-coding RNA HOTAIR promotes cervical cancer progression through regulating BCL2 via targeting miR-143-3p[J]. Cancer Biology & Therapy， 2018，19（5）：391-399.
[17]XIAO Z G， QU Z， CHEN Z K， et al. LncRNA HOTAIR is a prognostic biomarker for the proliferation and chemoresistance of colorectal cancer via MiR-203a-3p-mediated wnt/β-catenin signaling pathway[J]. Cellular Physiology and Biochemistry： International Journal of Experimental Cellular Physiology， Biochemistry， and Pharmacology， 2018，46（3）：1275-1285.
[18]LI W T， WANG B L， YANG C S， et al. MiR-613 promotes cell proliferation and invasion in cervical cancer via targeting PTPN9[J]. European Review for Medical and Pharmacological Sciences， 2018，22（13）：4107-4114.
[19]劉春杰，刘宇，邓学坤，等. miR-32通过调控PI3K/Akt信号通路影响骨肉瘤细胞的增殖[J]. 河北医科大学学报， 2018，39（6）：662-667.
[20]CAI H H， YAO J， AN Y， et al. LncRNA HOTAIR Acts a competing endogenous RNA to control the expression of notch3 via sponging miR-613 in pancreatic cancer[J]. Oncotarget， 2017，8（20）：32905-32917.
（本文编辑 于国艺）
方法 采用实时荧光定量聚合酶链反应（RT-qPCR）检测食管鳞癌细胞中HOTAIR和miR-613的表达情况，双荧光素酶报告基因实验检测HOTAIR和miR-613靶向关系，CCK-8法和流式细胞仪检测细胞增殖和凋亡。
结果 与其他食管鳞癌细胞相比，人食管鳞癌细胞株Eca-109细胞中HOTAIR表达最高而且miR-613表达水平最低（F=48.56、56.28，P<0.05）。HOTAIR可靶向调控miR-613的表达。下调HOTAIR的表达明显抑制了Eca-109细胞增殖，提高了细胞凋亡和miR-613表达水平（F=205.28～396.53，P<0.05）;抑制miR-613表达后，Eca-109细胞增殖能力明显增强，而细胞凋亡能力明显减弱（F=51.04、511.37，P<0.05）。
结论 下调HOTAIR可通过调控miR-613表达抑制食管鳞癌Eca-109细胞增殖并促进其凋亡。
[关键词] 食管鳞状细胞癌;HOX转录反义RNA;RNA，长链非编码;微RNAs;细胞增殖;细胞凋亡
[中图分类号] R735.1;R342.2
[文献标志码] A
[文章编号] 2096-5532（2021）05-0736-06
doi：10.11712/jms.2096-5532.2021.57.171
[开放科学（资源服务）标识码（OSID）]
[网络出版] https：//kns.cnki.net/kcms/detail/37.1517.r.20211029.1732.002.html;2021-11-02 13：27：02
EFFECT OF THE EXPRESSION OF HOX TRANSCRIPT ANTISENSE INTERGENIC RNA AND MICRORNA-613 ON THE PROLIFERATION AND APOPTOSIS OF ESOPHAGEAL SQUAMOUS CELL CARCINOMA CELLS
CHEN Zhijun， CAO Ke-
xin， ZHU Deqi， GAN Shaoyin， WANG Zhongmin
（Department of Thoracic Surgery， The First Affiliated Hospital of Xinxiang Medical University， Xinxiang 453100， China）
[ABSTRACT] Objective To investigate the regulatory role of HOX transcript antisense intergenic RNA （HOTAIR） and microRNA-613 （miR-613） in esophageal squamous cell carcinoma cells and their effect on cell proliferation and apoptosis.
Me-
thods Quantitative real-time PCR was used to measure the expression of HOTAIR and miR-613 in esophageal squamous cell carcinoma cells; dual luciferase reporter gene assay was used to detect the targeting relationship between HOTAIR and miR-613; CCK-8 assay and flow cytometry were used to measure cell proliferation and apoptosis.
Results Compared with other esophageal squamous cell carcinoma cell lines， the human esophageal squamous cell carcinoma cell line Eca-109 had the highest expression level of HOTAIR and the lowest expression level of miR-613 （F=48.56，56.28;P<0.05）. HOTAIR showed targeted regulation of miR-613 expression. Downregulation of HOTAIR expression significantly inhibited the proliferation of Eca-109 cells and increased cell apoptosis and the expression level of miR-613 （F=205.28-396.53，P<0.05）. After the expression of miR-613 was inhibited， Eca-109 cells showed a significant increase in proliferation and a significant reduction in apoptosis （F=51.04，511.37;P<0.05）. [10]KANG M， LI Y， ZHU S T， et al. MicroRNA-193b Acts as a tumor suppressor gene in human esophageal squamous cell carcinoma via target regulation of KRAS[J]. Oncology Letters， 2019，17（4）：3965-3973.
[11]刘灿，陈丹杰，余军林，等. 晚期食管鳞癌患者血清sPD-L1与组织PD-L1的表达及与预后的关系[J]. 郑州大学学报（医学版）， 2019，54（4）：500-503.
[12]张常，王新文，王亮，等. “垃圾”DNA的奥秘[J]. 科学通报， 2016，61（Z2）：3079-3084.
[13]ZHANG R， XIA L Q， LU W W， et al. LncRNAs and cancer[J]. Oncology Letters， 2016，12（2）：1233-1239.
[14]REDDY K B. MicroRNA （miRNA） in cancer[J]. Cancer Cell International， 2015，15：38.
[15]ZHAO W Y， GENG D H， LI S Q， et al. LncRNA HOTAIR influences cell growth， migration， invasion， and apoptosis via the miR-20a-5p/HMGA2 axis in breast cancer[J]. Cancer Medicine， 2018，7（3）：842-855.
[16]LIU M Z， JIA J Y， WANG X J， et al. Long non-coding RNA HOTAIR promotes cervical cancer progression through regulating BCL2 via targeting miR-143-3p[J]. Cancer Biology & Therapy， 2018，19（5）：391-399.
[17]XIAO Z G， QU Z， CHEN Z K， et al. LncRNA HOTAIR is a prognostic biomarker for the proliferation and chemoresistance of colorectal cancer via MiR-203a-3p-mediated wnt/β-catenin signaling pathway[J]. Cellular Physiology and Biochemistry： International Journal of Experimental Cellular Physiology， Biochemistry， and Pharmacology， 2018，46（3）：1275-1285.
[18]LI W T， WANG B L， YANG C S， et al. MiR-613 promotes cell proliferation and invasion in cervical cancer via targeting PTPN9[J]. European Review for Medical and Pharmacological Sciences， 2018，22（13）：4107-4114.
[19]劉春杰，刘宇，邓学坤，等. miR-32通过调控PI3K/Akt信号通路影响骨肉瘤细胞的增殖[J]. 河北医科大学学报， 2018，39（6）：662-667.
[20]CAI H H， YAO J， AN Y， et al. LncRNA HOTAIR Acts a competing endogenous RNA to control the expression of notch3 via sponging miR-613 in pancreatic cancer[J]. Oncotarget， 2017，8（20）：32905-32917.
（本文编辑 于国艺）