{"id":6494,"date":"2024-08-06T12:21:17","date_gmt":"2024-08-06T12:21:17","guid":{"rendered":"https:\/\/longchangextracts.com\/?p=6494"},"modified":"2024-08-06T12:21:17","modified_gmt":"2024-08-06T12:21:17","slug":"luteolin-inhibits","status":"publish","type":"post","link":"https:\/\/longchangextracts.com\/tr\/luteolin-inhibits\/","title":{"rendered":"Ribozomal protein S12 ekspresyonunun luteolin taraf\u0131ndan negatif d\u00fczenlenmesi MDA-MB-231 h\u00fccrelerinin \u00e7o\u011falmas\u0131n\u0131 ve istilas\u0131n\u0131 engeller"},"content":{"rendered":"

Ribozomal protein S12 ekspresyonunun luteolin taraf\u0131ndan negatif d\u00fczenlenmesi MDA-MB-231 h\u00fccrelerinin \u00e7o\u011falmas\u0131n\u0131 ve istilas\u0131n\u0131 engeller
\nLuteolin (Lut), karaci\u011fer kanseri ve meme kanseri gibi in vitro ve in vivo t\u00fcm\u00f6r deneylerinde iyi bir anti-t\u00fcm\u00f6r etkiye sahip oldu\u011fu kan\u0131tlanm\u0131\u015f do\u011fal bir flavonoid bile\u015fi\u011fidir. Ayr\u0131ca Lut, farkl\u0131 t\u00fcm\u00f6r h\u00fccrelerinin \u00e7o\u011falmas\u0131n\u0131 inhibe etmede ve apoptozlar\u0131n\u0131 ind\u00fcklemede nispeten d\u00fc\u015f\u00fck sitotoksisiteye sahiptir, bu da onu potansiyel bir anti-t\u00fcm\u00f6r ilac\u0131 haline getirir. Bu konuda yap\u0131lan \u00f6nceki deney, Lut'un PETN ekspresyonunu d\u00fczenleyerek PI3K\/Akt aktivitesini etkileyebilece\u011fini ve ard\u0131ndan meme kanseri h\u00fccrelerinin \u00e7o\u011falmas\u0131n\u0131 engelleyebilece\u011fini do\u011frulam\u0131\u015ft\u0131r. Bununla birlikte, meme kanserinin olu\u015fumu ve geli\u015fiminin \u00e7e\u015fitli d\u00fczenleyici mekanizmalara sahip oldu\u011fu d\u00fc\u015f\u00fcn\u00fcld\u00fc\u011f\u00fcnde, Lut'un meme kanseri h\u00fccrelerinin \u00e7o\u011falmas\u0131n\u0131 engellemek i\u00e7in ba\u015fka mekanizmalara sahip olup olmad\u0131\u011f\u0131 belirsizli\u011fini korumaktad\u0131r. Ribozomal protein (RP), ribozomlar\u0131n ana bile\u015fenlerinden biridir ve h\u00fccre i\u00e7i protein biyosentezi, transkripsiyon, translasyon ve di\u011fer d\u00fczenleyici molek\u00fcler ilgili b\u00f6lgelerde h\u00fccre \u00e7o\u011falmas\u0131nda rol oynar. Kolorektal kanser, mide kanseri, karaci\u011fer kanseri ve \u00f6zofagus kanserinde de\u011fi\u015fen derecelerde anormal ekspresyon g\u00f6sterir. Ribozomal protein S12 (RPS12) serviks kanseri hastalar\u0131nda y\u00fcksek oranda eksprese edilirken, normal dokularda ekspresyonu nispeten d\u00fc\u015f\u00fckt\u00fcr. Ayr\u0131ca, RPS12 mide kanseri dokusunda da a\u015f\u0131r\u0131 eksprese edilir ve t\u00fcm\u00f6r h\u00fccresi metastaz\u0131n\u0131 te\u015fvik edebilir. Bununla birlikte, RPS12 geninin meme kanseri h\u00fccrelerinin \u00e7o\u011falmas\u0131ndaki d\u00fczenleyici rol\u00fc a\u00e7\u0131k\u00e7a tan\u0131mlanmam\u0131\u015ft\u0131r. C-Myc, ribozom sentezi i\u00e7in d\u00fczenleyici bir fakt\u00f6rd\u00fcr. Fibroblastlar\u0131n cDNA mikroarray analizi yoluyla, h\u00fccrelerdeki RPS12 ekspresyon seviyesinin c-Myc ile ili\u015fkili olabilece\u011fi bulunmu\u015ftur. Bu \u00e7al\u0131\u015fma, meme kanserinin klinik tedavisinde ila\u00e7lar\u0131n geli\u015ftirilmesi ve se\u00e7imi i\u00e7in yeni fikirler sa\u011flamak amac\u0131yla, meme kanseri MDA-MB-231 h\u00fccrelerinin \u00e7o\u011falmas\u0131n\u0131 ve istilas\u0131n\u0131 engelleyen Lut s\u00fcrecinde c-Myc ve RPS12 mekanizmas\u0131n\u0131 ara\u015ft\u0131rmay\u0131 ama\u00e7lamaktad\u0131r.<\/p>\n

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\nSon y\u0131llarda t\u0131bbi seviyenin h\u0131zla geli\u015fmesine ra\u011fmen, meme kanserine y\u00f6nelik klinik tedavinin etkisi hala zay\u0131ft\u0131r. Bunun temel nedeni, t\u00fcm\u00f6r geli\u015fimi ve erken metastaz mekanizmas\u0131n\u0131n net olmamas\u0131d\u0131r. Do\u011fal bir flavonoid bile\u015fi\u011fi olan Lut, \u00e7e\u015fitli k\u00f6t\u00fc huylu t\u00fcm\u00f6rlerin olu\u015fumu ve geli\u015fimi \u00fczerinde inhibit\u00f6r etkilere sahiptir. Ara\u015ft\u0131rma grubumuz daha \u00f6nce Lut'un meme kanseri h\u00fccre proliferasyonu \u00fczerindeki inhibit\u00f6r etkisini do\u011frulam\u0131\u015f olsa da, spesifik mekanizmas\u0131 hen\u00fcz a\u00e7\u0131kl\u0131\u011fa kavu\u015fturulmam\u0131\u015ft\u0131r. Bu \u00e7al\u0131\u015fmada, Lut'un PI3K\/Akt\/mTOR sinyal yolunu inhibe ederek c-Myc ekspresyonunu azaltabildi\u011fini ve RPS12 ekspresyonunu negatif d\u00fczenleyerek meme kanseri MDA-MB-231 h\u00fccrelerinin proliferasyonunu ve invazyonunu inhibe etti\u011fini bulduk. Bu da Lut'un meme kanseri tedavisindeki potansiyelini do\u011frulam\u0131\u015ft\u0131r.
\nRibozomlar h\u00fccrelerde protein sentezi i\u00e7in ana organellerdir ve \u00f6karyotik ribozomlar yakla\u015f\u0131k 80 RP i\u00e7erir. RP'ler, rahim a\u011fz\u0131 kanseri ve mide kanseri gibi \u00e7e\u015fitli t\u00fcm\u00f6r h\u00fccrelerinde anormal \u015fekilde yukar\u0131 do\u011fru d\u00fczenlenir ve t\u00fcm\u00f6r h\u00fccrelerinin \u00e7o\u011falmas\u0131 ve istilas\u0131 ile ili\u015fkilidir. Ara\u015ft\u0131rmalar, RPS12'nin mide kanseri h\u00fccrelerindeki ifade seviyesinin normal h\u00fccrelerdekinden \u00f6nemli \u00f6l\u00e7\u00fcde daha y\u00fcksek oldu\u011funu g\u00f6stermi\u015ftir, bu da RPS12'nin mide kanserinin olu\u015fumunda ve geli\u015fiminde rol oynayabilece\u011fini d\u00fc\u015f\u00fcnd\u00fcrmektedir. Bu \u00e7al\u0131\u015fma, RPS12'nin meme kanseri h\u00fccre hatlar\u0131nda da y\u00fcksek oranda ifade edildi\u011fini ve bunun di\u011fer t\u00fcm\u00f6rlerle tutarl\u0131 oldu\u011funu bulmu\u015ftur. Bununla birlikte, meme kanseri h\u00fccreleri Lut ile muamele edildi\u011finde, RPS12'nin ekspresyon seviyesi \u00f6nemli \u00f6l\u00e7\u00fcde azalm\u0131\u015ft\u0131r. RPS12'nin meme kanseri h\u00fccrelerinde Lut'un d\u00fczenlenmesine de kat\u0131ld\u0131\u011f\u0131 do\u011fruland\u0131. RPS12'nin meme kanseri h\u00fccrelerinin g\u00f6\u00e7\u00fc ve istilas\u0131ndaki rol\u00fcn\u00fc daha da netle\u015ftirmek i\u00e7in, RPS12'nin susturulmas\u0131n\u0131n h\u00fccre istilas\u0131 ve g\u00f6\u00e7\u00fc \u00fczerindeki etkisini de test ettik. Sonu\u00e7lar, RPS12'nin susturulmas\u0131n\u0131n meme kanseri h\u00fccrelerinin istilas\u0131n\u0131 ve g\u00f6\u00e7\u00fcn\u00fc \u00f6nemli \u00f6l\u00e7\u00fcde engelleyebilece\u011fini g\u00f6sterdi. Bu ayn\u0131 zamanda meme kanserinde RPS12'nin y\u00fcksek ekspresyonunun t\u00fcm\u00f6r geli\u015fimi ve metastaz\u0131na katk\u0131da bulunabilece\u011fini g\u00f6stermektedir. c-Myc geni \u015fu anda h\u00fccre b\u00f6l\u00fcnmesini ve \u00e7o\u011falmas\u0131n\u0131 etkili bir \u015fekilde te\u015fvik edebilen bir proto onkogen olarak bilinmektedir ve \u00e7e\u015fitli malign t\u00fcm\u00f6rlerin olu\u015fumu ve geli\u015fimi ile yak\u0131ndan ili\u015fkilidir. Ara\u015ft\u0131rmalar, kolon kanserinde MicroRNA-184'\u00fcn kolon kanseri h\u00fccrelerinin \u00e7o\u011falmas\u0131n\u0131 engelleyebildi\u011fini ve c-Myc'nin ifade d\u00fczeyini a\u015fa\u011f\u0131 d\u00fczenleyerek h\u00fccre apoptozunu te\u015fvik edebildi\u011fini g\u00f6stermi\u015ftir. Ayr\u0131ca c-Myc, mide kanseri h\u00fccrelerinde de h\u00fccre \u00e7o\u011falmas\u0131 \u00fczerinde benzer bir te\u015fvik edici etkiye sahiptir. Bu \u00e7al\u0131\u015fma, c-Myc'nin meme kanseri h\u00fccre hatlar\u0131nda da y\u00fcksek oranda eksprese edildi\u011fini ve c-Myc ekspresyonunun a\u015fa\u011f\u0131 reg\u00fclasyonunun h\u00fccrelerde RPS12 ekspresyonunu ve transkripsiyonunu daha da inhibe edebilece\u011fini ve bunun da meme kanseri h\u00fccrelerinin proliferasyonunu daha da inhibe edebilece\u011fini bulmu\u015ftur. c-Myc'nin di\u011fer t\u00fcm\u00f6r h\u00fccrelerindeki rol\u00fc g\u00f6z \u00f6n\u00fcne al\u0131nd\u0131\u011f\u0131nda, Lut'un etkisini c-Myc\/RPS12 ekspresyonunu etkileyerek g\u00f6sterebilece\u011fi bir kez daha ortaya konmu\u015ftur.
\nPI3K\/Akt, t\u00fcm\u00f6r b\u00fcy\u00fcmesi ve farkl\u0131la\u015fmas\u0131 gibi s\u00fcre\u00e7lere kat\u0131labilen enzim aktif bir h\u00fccre i\u00e7i sinyal yoludur. \u00c7al\u0131\u015fmalar, PI3K\/Akt sinyal yolunun meme kanseri h\u00fccrelerinin \u00e7o\u011falmas\u0131 ve g\u00f6\u00e7\u00fc s\u0131ras\u0131nda genellikle anormal \u015fekilde aktive oldu\u011funu g\u00f6stermi\u015ftir. Bu \u00e7al\u0131\u015fmada, hem Akt inhibit\u00f6r\u00fc LY294002 hem de mTOR inhibit\u00f6r\u00fc rapamisin, mTOR ve S6K fosforilasyon seviyelerini \u00f6nemli \u00f6l\u00e7\u00fcde inhibe etmek i\u00e7in kullan\u0131lm\u0131\u015ft\u0131r. Ancak, rapamisinin Akt fosforilasyon seviyeleri \u00fczerinde \u00f6nemli bir etkisi olmam\u0131\u015ft\u0131r, \u00e7\u00fcnk\u00fc mTOR PI3K\/Akt'\u0131n a\u015fa\u011f\u0131 ak\u0131\u015f molek\u00fcl\u00fcd\u00fcr ve bu nedenle Akt fosforilasyonu \u00fczerinde etkisi yoktur. Ek olarak, PI3K\/Ak ve mTOR inhibit\u00f6rleri h\u00fccrelerde RPS12 ve c-Myc ekspresyonunu \u00f6nemli \u00f6l\u00e7\u00fcde azaltabilir ve b\u00f6ylece h\u00fccre proliferasyonunu inhibe edebilir. Bu sonu\u00e7lar, RPS12 ve c-Myc'nin ayn\u0131 zamanda PI3K\/Akt\/mTOR sinyal yolunun a\u015fa\u011f\u0131 ak\u0131\u015f molek\u00fclleri olabilece\u011fini ve meme kanseri h\u00fccrelerinin \u00e7o\u011falmas\u0131 ve g\u00f6\u00e7\u00fc \u00fczerinde Lut'un d\u00fczenlenmesine kat\u0131labilece\u011fini g\u00f6stermektedir.
\n\u00d6zetle, Lut, PI3K\/Akt\/mTOR sinyal yolunu inhibe ederek meme kanseri MDA-MB-231 h\u00fccrelerinin proliferasyonunu ve invazyonunu inhibe edebilir, b\u00f6ylece c-Myc ekspresyonunu a\u015fa\u011f\u0131 reg\u00fcle edebilir ve ard\u0131ndan RPS12'yi negatif olarak d\u00fczenleyebilir. Bu sonu\u00e7lar, RPS12 ve c-Myc'nin meme kanseri tedavisi i\u00e7in potansiyel hedefler olabilece\u011fini ve Lut'un RPS12 ve c-Myc ekspresyonunu d\u00fczenleyerek anti-t\u00fcm\u00f6r bir rol oynayabilece\u011fini g\u00f6stermektedir. Bu, meme kanserinin klinik tedavisi i\u00e7in yeni fikirler sa\u011flayacakt\u0131r.<\/p>","protected":false},"excerpt":{"rendered":"

Negative regulation of ribosomal protein S12 expression by luteolin inhibits proliferation and invasion of MDA-MB-231 cells Luteolin (Lut) is a natural flavonoid compound, which has been proved to have a good anti-tumor effect in in vitro and in vivo tumor experiments such as liver cancer and breast cancer. In addition, Lut has relatively low cytotoxicity […]<\/p>","protected":false},"author":1,"featured_media":0,"comment_status":"closed","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[20],"tags":[],"yoast_head":"\nNegative regulation of ribosomal protein S12 expression by luteolin inhibits proliferation and invasion of MDA-MB-231 cells - China Chemical Manufacturer<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/longchangextracts.com\/tr\/luteolin-inhibits\/\" \/>\n<meta property=\"og:locale\" content=\"tr_TR\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Negative regulation of ribosomal protein S12 expression by luteolin inhibits proliferation and invasion of MDA-MB-231 cells - China Chemical Manufacturer\" \/>\n<meta property=\"og:description\" content=\"Negative regulation of ribosomal protein S12 expression by luteolin inhibits proliferation and invasion of MDA-MB-231 cells Luteolin (Lut) is a natural flavonoid compound, which has been proved to have a good anti-tumor effect in in vitro and in vivo tumor experiments such as liver cancer and breast cancer. 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