Abstract
MicroRNAs (miRNAs) often display different expression in many cancers and other diseases in current research studies. miR-223 expression is upregulated in rheumatoid arthritis. Also, miR-223 expression has been demonstrated to be highly expressed in pancreatic cancer and gastric cancer in comparison with normal tissue. However, whether miR-223 displays different expression in ovarian cancer and what its underlying functions are in ovarian cancer have remained unclear. In this study, we demonstrated that miR-223-3p was upregulated in ovarian cancer tissue. Next, we explored the functional role of miR-223-3p in ovarian cancer using SKOV3 and OVCAR3 cell lines. Our results suggested that miR-223-3p mimic promoted ovarian cancer cell proliferation, migration, and invasion in vitro. However, miR-223-3p inhibitor displayed the opposite effects. In addition, we demonstrated that miR-223-3p mimic promoted tumor growth in vivo. Furthermore, we found SOX11 (sex determining region Y-box 11) was inversely expressed with miR-223-3p in ovarian cancer (OC) cell lines and tissue specimens. miR-223-3p mimic decreased SOX11 expression. Overexpressing SOX11 inhibited ovarian cancer cell proliferation and invasion, which indicated that miR-223-3p regulated OC cell proliferation and invasion through targeting SOX11 expression. In conclusion, the findings of the present study demonstrated that miR-223-3p could be a potential therapeutic for ovarian cancer.
Highlights
Ovarian cancer is the most lethal of all gynecological tumors in the world [1,2]
Wei, Y. et al found that miR-223-3p promotes the biological behavior of prostate cancer by targeting SPET6 [14] and Zhang, J. et al indicated that microRNA-223 is an oncogene in human colorectal cancer cells, and the silencing of miR-223 by miR-223-inhibitor can suppress cell proliferation, migration, and invasion of colorectal cancer cells [16]
We found an overexpression of miR-223-3p in ovarian cancer cell lines (SKOV3, OVCAR3, A2780, ES2) compared with the normal ovarian cell line
Summary
Ovarian cancer is the most lethal of all gynecological tumors in the world [1,2]. Current treatments have significantly improved ovarian cancer patients’ quality of life, but the 5-year survival rate is still 35–38% [3,4] because of recurrence and metastasis. Recent studies have demonstrated that miR-223 influences the biological progression of various cancer cells [12]. Mef2c-β-catenin pathway, miR-223 affected the invasion of breast cancer cells [13]. MiR-223 has been reported to reinforce prostate cancer cell biological behaviors [14], increase the proliferation and migrInat.tiJ.oMnolo. EIrnmcoorne,clwuesifoonu,nodumr idRa-2ta23i-n3dpicates that miRi-n2h2i3b-it3opr ihnacsreaaspedotgeennteiasloxth11er(asepxeduettiecrmtairngientgrroelgeiofnorYo-bvoaxr1ia1n) ecxapnrecsesri.on and overexpression of sox has negative effects on ovarian cancer cell proliferation, migration, and invasion. MiR-22.2R3e-s3upltWs as Upregulated in (Ovarian Cancer) OC Cell Lines and Tissue Specimens. TThhee eeffffeecctt of miR-222233--33pp innhhiibbiittoorr oonn thhee sox1111 transsllaattiioonn wwaass ddeetteecctteedd bbyy luucciiffeerraassee rreeppoorrtteerr aassssaayy in SKOV3 cells. MiR-223-3p inhibitor increased SOX11 expression (Figure 4B). SOX11 Was Inversely Expressed with miR-223-3p in OC Cell Lines and Tissue Specimens. TmTooiRe-xe2px2pl3ol-ro3erpetMhetihmtehiecrtIhanpecreraeuaptsieecudetSfifcKecOetfVofe3fcmEt niRogrf-a2f2mt3edi-R3Tp-2uo2mn3o-Or3spCGgroornwowtOhthCingvroivwot,hweininvoivcuol,atwede3i×n1o0c6umlaitRed2323×-31pT0os6cemrxapimRlob-2rlee2/3tmh-3eipmthiscecrrtaarpamnebusflteeicc/temefdfiemcStKicoOftrmVa3inRsc-fe2el2lcs3te-s3dupbSocKunOtOaVnCe3gocrueoslwllysthisnuinbthcvueivtraoing, hewoteuflisanlnyokciusnloatftheBedAr3iBg×Lh1/tc06flmmainicRke-.s To2uf2m3B-oA3rpBs Lsgc/rrcaemwmbilfceae/s.mteirmTuiicmn tortarhsnesgfmerecitwRed-2faS2s3Kt-Oe3rpVi3nmcitemhllesicsmutbirRacn-u2st2afe3nc-e3toepudsmlgyirmionuictphtercaronimgshfpetacfrtlieandngkgstrooofutBphAecBosLmc/rcpammaribicnleeg. ttrToauntmshfeeocrtsecdrgarmgerwboluefpatsr(taFenrigsfuienrcetteh7dAe g)m.roAiuRtp-2th2(3Fe-i3gfpiunraeml i7emAxpi)c.erAtirmat netnshfte, cifitnendcarelgaersoxeupdpertuicmmoemonrpt,asriizinnecgraenatodsedtwheetuigsmhcrtoarwmsebirzleee oatbnrsadenrswvfeeedcitgehidnt gwthreoeruepmoi(bRFs-ie2gr2uv3re-e3dp7iAnm).tihmAeitcmthtiRrea-n2fis2nf3ea-cl3tpeedxmpgeimrriomiuceptnrta(,Fniisgnfucerrceetaesd7eAdg,rBtou)u.mpToh(rFeinsgi,zuewreaen7Acda,rBwr)ie.eidTghoteunwt, ewarnee icmoabmrrsieuerndvoeohduistitnoacnhtheiemmmistuirRny-o2(Ih2H3is-Ct3o)pcahnmedmimwisiectsrtyetrra(nInHbsflCoe)cttaaesndsdagywrtooeusdpteetr(enFcitbgSluoOrteXa17s1sAae,yxBp)t.roeTsdhseieotnen,c.tAwSseOsXhcao1rw1rinexdinproFeuisgtsuioarne . 7AiCms,Dsmh,uothnweonhpirsnototFeciihgneuemrxeips7rtCreys,Ds(iIo,HtnhCoe)fpaSnrOodtXew1ine1sewtexarpnsredbsleoscitroaensassoaefydStOionXdthe1t1eewcmtaiSRsO-d2Xe21c31r-e3eapxspmerdeismisniiocthntr.eaAmnssisfReh-co2twe2d3n-g3inrpoFmuigpimu. riec t7raCn,Dsf,etchtedpgroroteuipn.expression of SOX11 was decreased in the miR-223-3p mimic transfected group
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