长链非编码RNA LINC00973对上皮性卵巢癌迁移、侵袭和远端转移的促进作用及其分子机制

doi:10.13481/j.1671-587X.20250402

吉林大学学报(医学版) ›› 2025, Vol. 51 ›› Issue (4): 866-878.doi: 10.13481/j.1671-587X.20250402

长链非编码RNA LINC00973对上皮性卵巢癌迁移、侵袭和远端转移的促进作用及其分子机制

夏云秀^1,²,张硕^1,²,张桓海³,王飞²,董洪亮²(),杜静^1,²()

^1.滨州医学院附属医院妇科，山东滨州 256600
^2.滨州医学院附属医院医学研究中心，山东滨州 256600
^3.滨州医学院烟台附属医院甲状腺乳腺外科，山东烟台 264100

收稿日期:2024-09-08 接受日期:2024-10-24 出版日期:2025-07-28 发布日期:2025-08-25
通讯作者: 董洪亮,杜静 E-mail:hongliang.234@163.com;djedith@126.com
作者简介:夏云秀（1998-），女，山东省日照市人，在读硕士研究生，主要从事肿瘤发生发展机制方面的研究。
基金资助:
国家自然科学基金资助项目(82373097);山东省科技厅泰山学者人才项目(tsqn202103191)

Long non-coding RNA LINC00973 promotes migration, invasion and distal metastasis of epithelial ovarian cancer and its molecular mechanism

Yunxiu XIA^1,²,Shuo ZHANG^1,²,Huanhai ZHANG³,Fei WANG²,Hongliang DONG²(),Jing DU^1,²()

^1.Department of Gynecology，Affiliated Hospital，Binzhou Medical University，Binzhou 256603，China
^2.Medical Research Center，Affiliated Hospital，Binzhou Medical University，Binzhou 256603，China
^3.Department of Thyroid and Breast Surgery，Yantai Affiliated Hospital，Binzhou Medical University，Yantai 264100，China

Received:2024-09-08 Accepted:2024-10-24 Online:2025-07-28 Published:2025-08-25
Contact: Hongliang DONG,Jing DU E-mail:hongliang.234@163.com;djedith@126.com

摘要/Abstract

摘要：

目的探讨长链非编码RNA（lncRNA）LINC00973对上皮性卵巢癌迁移、侵袭和远端转移的影响，并阐明其分子机制。方法将人卵巢癌SKOV3和OVCAR3细胞分为EF1a-FH空载体对照组、LINC00973 OE组、U6-shRNA空载体对照组（SHV组）和LINC00973 KD组。分别转染插入无义序列的pLent-EF1a-FH-CMV-copGFP-P2A-Puro、LINC00973过表达、插入无义序列的pLent-U6-shRNA-CMV-copGFP-P2A-Puro和LINC00973小发夹RNA（shRNA）慢病毒，经嘌呤霉素筛选得到稳定转染的SKOV3和OVCAR3细胞。采用实时荧光定量PCR（RT-qPCR）法检测各组细胞中目的基因mRNA表达水平，细胞划痕实验检测各组细胞迁移率，Transwell小室实验检测各组细胞穿膜细胞数。小鼠腹腔注射SKOV3野生型（WT组）、LINC00973 OE（LINC00973 OE组）和LINC00973 KD（LINC00973 KD组）细胞，构建上皮性卵巢癌腹腔种植转移模型，采用HE染色观察各组小鼠结肠和肝脏组织形态表现，RNA测序（RNA-seq）分析SHV和LINC00973 KD组SKOV3细胞差异基因，RT-qPCR法检测正常卵巢上皮细胞IOSE-80和上皮性卵巢癌SKOV3、A2780及OVCAR3细胞中LINC00973 mRNA表达水平，各组细胞中LINC00973、波形蛋白（Vimentin），蜗牛家族转录因子1（Snail）、Twist家族碱性螺旋-环-螺旋转录因子1（Twist）、锌指E盒结合蛋白1（ZEB1）、锌指E盒结合蛋白2（ZEB2），趋化因子CXCL8和基质金属蛋白酶（MMP）16 mRNA表达水平及各组小鼠肝脏和结肠组织中LINC00973、Vimentin和Twist mRNA表达水平。结果与正常卵巢上皮IOSE-80细胞比较，上皮性卵巢癌SKOV3、OVCAR3和A2780细胞中LINC00973 mRNA表达水平均明显升高（P<0.01），SKOV3和OVCAR3细胞中LINC00973 mRNA表达水平最高，因此选择该2种细胞进行后续实验。SKOV3和OVCAR3细胞中，与对照组比较，LINC00973 OE组细胞中LINC00973 mRNA表达水平升高（P<0.01）；与SHV组比较，LINC00973 KD组细胞中LINC00973 mRNA表达水平降低（P<0.05或P<0.01），表明SKOV3和OVCAR3 LINC00973过表达及敲低细胞系构建成功。在SKOV3细胞中，与对照组比较，LINC00973 OE组细胞中Vimentin和Twist mRNA表达水平升高（P<0.05或P<0.01），Snail mRNA表达水平差异无统计学意义（P>0.05）；与SHV组比较，LINC00973 KD组细胞中Vimentin、Snail和Twist mRNA表达水平降低（P<0.01）。在OVCAR3细胞中，与对照组比较，LINC00973 OE组细胞中Vimentin、Snail和Twist mRNA表达水平升高（P<0.01）；与SHV组比较，LINC00973 KD组细胞中Vimentin、Snail和Twist mRNA表达水平降低（P<0.01）。细胞划痕实验，在SKOV3和OVCAR3细胞中，与对照组比较，LINC00973 OE组细胞划痕愈合率均明显升高（P<0.01）；与SHV组比较，LINC00973 KD组细胞划痕愈合率均明显降低（P<0.01）。Transwell小室实验，在SKOV3和OVCAR3细胞中，与对照组比较，LINC00973 OE组穿膜细胞数均明显增加（P<0.01）；与SHV组比较，LINC00973 KD组穿膜细胞数均明显减少（P<0.01）。与WT组比较，LINC00973 OE组小鼠腹腔形成的结节数增多，肝脏表面粗糙，有多处结节形成，肠系膜和结肠表面也有结节形成，结肠组织中LINC00973、Vimentin和Twist mRNA表达水平均升高（P<0.01）；与WT组比较，LINC00973 KD组小鼠腹腔无结节形成，肝脏表面光滑、无结节，且肝脏组织中LINC00973、Vimentin和Twist mRNA表达水平降低（P<0.01），肠系膜和结肠表面也无结节形成。HE染色，与WT组比较，LINC00973 OE组小鼠肝脏和结肠出现多处病变，表现为细胞大小不一、形状不规则、细胞边界不清，细胞核分裂增多，细胞质出现深浅不一的红色；LINC00973 KD组小鼠肝脏和结肠组织细胞排列整齐、形状规则，细胞核和细胞质分布均匀。RNA-seq测序，与SHV组比较，LINC00973 KD组未富集到与肿瘤转移相关的关键信号通路，而与肿瘤转移相关的基因CXCL8、MMP16、ZEB1和ZEB2转录水平降低。RT-qPCR法，与对照组比较，LINC00973 OE组细胞中ZEB1、ZEB2、CXCL8和MMP16 mRNA表达水平明显升高（P<0.01）；与SHV组比较，LINC00973 KD组细胞中ZEB1、ZEB2、CXCL8和MMP16的mRNA表达水平明显降低（P<0.01）。结论 LINC00973可以上调转移相关因子Vimentin、Snail、Twist、 ZEB1、 ZEB2、CXCL8和MMP16表达，促进上皮性卵巢癌的迁移、侵袭和远端转移。

关键词: 卵巢肿瘤, 转移, LINC00973, 实时荧光定量PCR, 基质金属蛋白酶

Abstract:

Objective To discuss the effect of long non-coding RNA（lncRNA） LINC00973 on the migration， invasion， and distant metastasis of epithelial ovarian cancer， and to clarify its molecular mechanism. Methods The human ovarian cancer SKOV3 and OVCAR3 cells were divided into EF1a-FH empty vector control group （control group）， LINC00973 overexpression group （LINC00973 OE group）， U6-shRNA empty vector control group （SHV group）， and LINC00973 knockdown group （LINC00973 KD group）， and were transfected with lentivirus containing nonsense sequence （pLent-EF1a-FH-CMV-copGFP-P2A-Puro）， LINC00973 overexpression， nonsense sequence （pLent-U6-shRNA-CMV-copGFP-P2A-Puro） and LINC00973 shRNA， respectively， followed by puromycin screening to obtain stably transfected SKOV3 and OVCAR3 cells. Real-time fluorescence quantitative PCR（RT-qPCR） method was used to detect the mRNA expression levels of target genes in the cells in various groups； wound healing assay was used to detect the migration rate of the cells in various groups； Transwell chamber assay was used to detect the number of transmembrane cells in various groups； The mice were divided into control group （WT group）， LINC00973 OE group， and LINC00973 KD group， with 4 mice in each group. SKOV3 wild-type cells， LINC00973 OE cells， and LINC00973 KD cells were intraperitoneally injected into the mice in various groups， respectively， to establish the epithelial ovarian cancer intraperitoneal implantation and metastasis model； HE staining was used to observe the morphology of the colon and liver tissues of the mice in various groups； RNA-secquencing （RNA-seq） was used to analyze the differentially expressed genes between SHV and LINC00973 KD groups in the SKOV3 cell line； RT-qPCR method was used to detect the mRNA expression levels of LINC00973 in the normal ovarian epithelial cells IOSE-80 and epithelial ovarian cancer cells SKOV3， A2780 and OVCAR3， the mRNA expression levels of LINC00973， Vimentin， Snail family transcriptional repressor 1 （Snail）， Twist family basic helix-loop-helix transcription factor 1 （Twist）， zinc finger E-box binding homeobox 1 （ZEB1）， zinc finger E-box binding homeobox 2 （ZEB2）， CXCL8 and matrix metalloproteinase （MMP） 16 in the cells in various groups， and the mRNA expression levels of LINC00973， Vimentin and Twist in liver and colon tissues of the mice in various groups. Results Compared with normal ovarian epithelial cells IOSE-80， the expression level of LINC00973 mRNA in the epithelial ovarian cancer cells SKOV3， OVCAR3 and A2780 was significantly increased （P<0.01）， with the highest expression level of LINC00973 in SKOV3 and OVCAR3 cells， which were therefore selected for subsequent experiments. In SKOV3 and OVCAR3 cells， compared with control group， the expression level of LINC00973 mRNA in the cells in LINC00973 OE group was increased （P<0.01）； compared with SHV group， the expression level of LINC00973 mRNA in the cells in LINC00973 KD group was decreased （P<0.05 or P<0.01）， indicating successful construction of LINC00973 overexpression and knockdown cell lines. In SKOV3 cells， compared with control group， the mRNA expression levels of Vimentin and Twist in LINC00973 OE group were increased （P<0.05 or P<0.01）， while no significant difference was observed in Snail mRNA expression level（P>0.05）； compared with SHV group， the mRNA expression levels of Vimentin， Snail and Twist in LINC00973 KD group were decreased （P<0.01）. In OVCAR3 cells， compared with control group， the mRNA expression levels of Vimentin， Snail and Twist in LINC00973 OE group were increased （P<0.01）； compared with SHV group， the expression levels of Vimentin， Snail， and mRNA Twist in LINC00973 KD group were decreased （P<0.01）. The wound healing assay results showed that compared with control group， the wound healing rates of the SKOV3 and OVCAR3 cells in LINC00973 OE group were significantly increased （P<0.01）； compared with SHV group， the wound healing rates of the cells in LINC00973 KD group were significantly decreased （P<0.01）. The Transwell chamber assay results showed that compared with control group， the numbers of transmembrane cells of the SKOV3 and OVCAR3 cells in LINC00973 OE group were significantly increased （P<0.01）； compared with SHV group， the numbers of transmembrane cells in LINC00973 KD group were significantly decreased （P<0.01）. Compared with WT group， the number of peritoneal nodules in LINC00973 OE group was increased， with rough liver surface and multiple nodules formed on mesentery and colon surface， and the expression levels of LINC00973， Vimentin， and Twist mRNA in colon tissue were increased （P<0.01）； compared with WT group， no nodules were formed in the peritoneal cavity of LINC00973 KD group， with smooth liver surface， no nodules in liver tissue， and decreased expression levels of LINC00973， Vimentin， and Twist mRNA， and no nodules were observed on mesentery and colon surface. The HE staining results showed that compared with WT group， the multiple lesions were observed in liver and colon tissues in LINC00973 OE group， manifested as uneven cell size， irregular shape， unclear cell boundaries， increased nuclear division， and uneven red staining in cytoplasm， while in LINC00973 KD group， the cells in liver and colon tissues were arranged neatly with regular shape， and uniform distribution of nuclei and cytoplasm. The RNA-seq results showed that compared with SHV group， no key signaling pathways related to tumor metastasis were enriched in LINC00973 KD group， and the transcription levels of metastasis-related genes CXCL8， MMP16， ZEB1， and ZEB2 were decreased. The RT-qPCR results showed that compared with control group， the expression levels of ZEB1， ZEB2， CXCL8， and MMP16 mRNA in the cells in LINC00973 OE group were significantly increased （P<0.01）； compared with SHV group， the expression levels of ZEB1， ZEB2， CXCL8， and MMP16 mRNA in the cells in LINC00973 KD group were significantly decreased （P<0.01）. Conclusion LINC00973 can up-regulate the expression of metastasis-related factors Vimentin， Snail， Twist， ZEB1， ZEB2， CXCL8， and MMP16， and promote the migration， invasion， and distant metastasis of epithelial ovarian cancer.

Key words: Ovarian neoplasm, Neoplasm metastasis, LINC00973, Real-time fluorescence quantitative PCR, Matrix metalloproteinases

中图分类号:

R737.31

夏云秀,张硕,张桓海,王飞,董洪亮,杜静. 长链非编码RNA LINC00973对上皮性卵巢癌迁移、侵袭和远端转移的促进作用及其分子机制[J]. 吉林大学学报(医学版), 2025, 51(4): 866-878.

Yunxiu XIA,Shuo ZHANG,Huanhai ZHANG,Fei WANG,Hongliang DONG,Jing DU. Long non-coding RNA LINC00973 promotes migration, invasion and distal metastasis of epithelial ovarian cancer and its molecular mechanism[J]. Journal of Jilin University(Medicine Edition), 2025, 51(4): 866-878.

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参考文献 35

[1]	WEBB P M， JORDAN S J. Global epidemiology of epithelial ovarian cancer［J］. Nat Rev Clin Oncol， 2024， 21（5）： 389-400.
[2]	TORRE L A， TRABERT B， DESANTIS C E， et al. Ovarian cancer statistics， 2018［J］. CA A Cancer J Clin， 2018， 68（4）： 284-296.
[3]	BRIDGES M C， DAULAGALA A C， KOURTIDIS A. LNCcation： lncRNA localization and function［J］. J Cell Biol， 2021， 220（2）： e202009045.
[4]	ZHANG Q， WU E Z， TANG Y H， et al. Deeply mining a universe of peptides encoded by long noncoding RNAs［J］. Mol Cell Proteomics， 2021， 20： 100109.
[5]	HERMAN A B， TSITSIPATIS D， GOROSPE M. Integrated lncRNA function upon genomic and epigenomic regulation［J］. Mol Cell， 2022， 82（12）： 2252-2266.
[6]	HE S L， CHEN Y L， CHEN Q H， et al. LncRNA KCNQ1OT1 promotes the metastasis of ovarian cancer by increasing the methylation of EIF2B5 promoter［J］. Mol Med， 2022， 28（1）： 112.
[7]	YU X， ZHAO P F， LUO Q Y， et al. RUNX1-IT1 acts as a scaffold of STAT1 and NuRD complex to promote ROS-mediated NF-κB activation and ovarian cancer progression［J］. Oncogene， 2024， 43（6）： 420-433.
[8]	LIN H， XU X， CHEN K L， et al. LncRNA CASC15， miR-23b cluster and SMAD3 form a novel positive feedback loop to promote epithelial-mesenchymal transition and metastasis in ovarian cancer［J］. Int J Biol Sci， 2022， 18（5）： 1989-2002.
[9]	KARPOV D S， SPIRIN P V， ZHELTUKHIN A O， et al. LINC00973 induces proliferation arrest of drug-treated cancer cells by preventing p21 degradation［J］. Int J Mol Sci， 2020， 21（21）： 8322.
[10]	ZINOVIEVA O L， GRINEVA E N， PROKOFJEVA M M， et al. Expression of long non-coding RNA LINC00973 is consistently increased upon treatment of colon cancer cells with different chemotherapeutic drugs［J］. Biochimie， 2018， 151： 67-72.
[11]	LIU Y B， LI X Z， ZHANG C M， et al. LINC00973 is involved in cancer immune suppression through positive regulation of Siglec-15 in clear-cell renal cell carcinoma［J］. Cancer Sci， 2020， 111（10）： 3693-3704.
[12]	GUO Q， LI D， LUO X Y， et al. The regulatory network and potential role of LINC00973-miRNA-mRNA ceRNA in the progression of non-small-cell lung cancer［J］. Front Immunol， 2021， 12： 684807.
[13]	TADIĆ V， ZHANG W， BROZOVIC A. The high-grade serous ovarian cancer metastasis and chemoresistance in 3D models［J］. Biochim Biophys Acta Rev Cancer， 2024， 1879（1）： 189052.
[14]	CAI Y S， LYU T， LI H， et al. LncRNA CEBPA-DT promotes liver cancer metastasis through DDR2/β-catenin activation via interacting with hnRNPC［J］. J Exp Clin Cancer Res， 2022， 41（1）： 335.
[15]	XIU B Q， CHI Y Y， LIU L， et al. LINC02273 drives breast cancer metastasis by epigenetically increasing AGR2 transcription［J］. Mol Cancer， 2019， 18（1）： 187.
[16]	WANG Y， LIU F， CHEN L， et al. Neutrophil extracellular traps （NETs） promote non-small cell lung cancer metastasis by suppressing lncRNA MIR503HG to activate the NF-κB/NLRP3 inflammasome pathway［J］. Front Immunol， 2022， 13： 867516.
[17]	HU H F， HAN L， FU J Y， et al. LINC00982-encoded protein PRDM16-DT regulates CHEK2 splicing to suppress colorectal cancer metastasis and chemoresistance［J］. Theranostics， 2024， 14（8）： 3317-3338.
[18]	TONG L L， WANG Y Y， AO Y， et al. CREB1 induced lncRNA HAS2-AS1 promotes epithelial ovarian cancer proliferation and invasion via the miR-466/RUNX2 axis［J］. Biomed Pharmacother， 2019， 115： 108891.
[19]	LIU J， ZHU Y， WANG H， et al. LINC00629， a HOXB4-downregulated long noncoding RNA， inhibits glycolysis and ovarian cancer progression by destabilizing c-Myc［J］. Cancer Sci， 2024， 115（3）： 804-819.
[20]	LI Y， LOU S H， ZHANG J， et al. m⁶A methylation-mediated regulation of LncRNA MEG3 suppresses ovarian cancer progression through miR-885-5p and the VASH1 pathway［J］. J Transl Med， 2024， 22（1）： 113.
[21]	FARDI M， ALIVAND M， BARADARAN B， et al. The crucial role of ZEB2： from development to epithelial-to-mesenchymal transition and cancer complexity［J］. J Cell Physiol， 2019， 234（9）： 14783-14799.
[22]	SáNCHEZ-TILLó E， PEDROSA L， VILA I， et al. The EMT factor ZEB1 paradoxically inhibits EMT in BRAF-mutant carcinomas［J］. JCI Insight， 2023， 8（20）：e164629.
[23]	POULIQUEN D L， BOISSARD A， HENRY C， et al. Curcuminoids as modulators of EMT in invasive cancers： a review of molecular targets with the contribution of malignant mesothelioma studies［J］. Front Pharmacol， 2022， 13： 934534.
[24]	SUN Z Q， SHAO B， LIU Z Q， et al. LINC01296/miR-141-3p/ZEB1-ZEB2 axis promotes tumor metastasis via enhancing epithelial-mesenchymal transition process［J］. J Cancer， 2021， 12（9）： 2723-2734.
[25]	LI Y Y， FEI H， LIN Q W， et al. ZEB2 facilitates peritoneal metastasis by regulating the invasiveness and tumorigenesis of cancer stem-like cells in high-grade serous ovarian cancers［J］. Oncogene， 2021， 40（32）： 5131-5141.
[26]	TATTI O， GUCCIARDO E， PEKKONEN P， et al. MMP16 mediates a proteolytic switch to promote cell-cell adhesion， collagen alignment， and lymphatic invasion in melanoma［J］. Cancer Res， 2015， 75（10）： 2083-2094.
[27]	YAN P F， WANG J， LIU H Y， et al. M1 macrophage-derived exosomes containing miR-150 inhibit glioma progression by targeting MMP16［J］. Cell Signal， 2023， 108： 110731.
[28]	YANG F Q， ZHANG J Q， JIN J J， et al. HOXA11-AS promotes the growth and invasion of renal cancer by sponging miR-146b-5p to upregulate MMP16 expression［J］. J Cell Physiol， 2018， 233（12）： 9611-9619.
[29]	LI Y Y， WANG Y， YU L， et al. miR-146b-5p inhibits glioma migration and invasion by targeting MMP16［J］. Cancer Lett， 2013， 339（2）： 260-269.
[30]	LIU Q， LI A P， TIAN Y J， et al. The CXCL8-CXCR1/2 pathways in cancer［J］. Cytokine Growth Factor Rev， 2016， 31： 61-71.
[31]	PIAO H Y， FU L F， WANG Y X， et al. A positive feedback loop between gastric cancer cells and tumor-associated macrophage induces malignancy progression［J］. J Exp Clin Cancer Res， 2022， 41（1）： 174.
[32]	FU X R， WANG Q M， DU H， et al. CXCL8 and the peritoneal metastasis of ovarian and gastric cancer［J］. Front Immunol， 2023， 14： 1159061.
[33]	ZHANG N， LIU Y Y， WANG Y Y， et al. Decitabine reverses TGF-β1-induced epithelial-mesenchymal transition in non-small-cell lung cancer by regulating miR-200/ZEB axis［J］. Drug Des Devel Ther， 2017， 11： 969-983.
[34]	CHOI P W， NG S W. The functions of microRNA-200 family in ovarian cancer： beyond epithelial-mesenchymal transition［J］. Int J Mol Sci， 2017， 18（6）： 1207.
[35]	ZHAO M N， ZHANG L F， SUN Z， et al. A novel microRNA-182/Interleukin-8 regulatory axis controls osteolytic bone metastasis of lung cancer［J］. Cell Death Dis， 2023， 14（5）： 298.

Gene	Primer（5'-3'）
LINC00973	F: CAAGGACAATTATTCCCTCAC R: GACAAAGCCAAGGATTCAGT
Vimentin	F: CGCCAACTACATCGACAAGGTGC R: CTGGTCCACCTGCCGGCGCAG
Snail	F: TCCACGAGGTGTGACTAACT R: CCGACAAGTGACAGCCATTA
Twist	F: CTAGAGACTCTGGAGCTGGATA R: TCTGGGAATCACTGTCCACG
ZEB1	F: AAGTGGCGGTAGATGGTA R: TGTTGTATGGGTGAAGCA
ZEB2	F: TCTGCGACATAAATACGA R: GAGTGAAGCCTTGAGTGC
MMP16	F: TGTGATGGACCAACAGAC R: ATACAAGAGGCATAAGG
CXCL8	F: CTAGTTTGATACTCCCAGTC R: AAGTTTCAACCAGCAAGA
GAPDH	F: CTCCTCCTGTTCGACAGTCAGC R: CCCAATACGACCAAATCCGTT

Group	Expression level of LINC00973
IOSE-80	1.000±0.019
SKOV3	211.916±15.037^*
OVCAR3	82.331±0.051^*
A2780	69.105±1.297^*
F	22.460
P	<0.01

Group	LINC00973
Control	1.001±0.049
LINC00973 OE	448.815±24.601^*
SHV	1.001±0.047
LINC00973 KD	0.351±0.024^△

Group	LINC00973
Control	1.003±0.074
LINC00973 OE	206.375±25.735^*
SHV	1.001±0.039
LINC00973 KD	0.696±0.060^△

长链非编码RNA LINC00973对上皮性卵巢癌迁移、侵袭和远端转移的促进作用及其分子机制

Long non-coding RNA LINC00973 promotes migration, invasion and distal metastasis of epithelial ovarian cancer and its molecular mechanism

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