I-World Health Organization ihlela ukuthi kusukela ngo-2030, abantu abangaphezu kwesigidi bazobulawa umdlavuza wesibindi unyaka ngamunye. I-Cold Spring Harbour Laboratory (CSHL) USolwazi Adrian Krainer, owake waba ngu-postdoc Wai Kit Ma, kanye no-Dillon Voss, waseStony Brook University MD-Ph.D. abafundi abahlala kulebhu yaseKrainer, baqhamuke nendlela yokuphazamisa indlela yamandla evumela ukuthi lo mdlavuza ukhule futhi usabalale. Basanda kushicilela umsebenzi wabo, obekusebenzisana ne-Ionis Pharmaceuticals, kumagazini iCancer Research.
Ososayensi be-CSHL basebenzise i-antisense oligonucleotides (ASOs), okuyinhlanganisela yokwenziwa yekhodi yofuzo ebophezela ku-RNA futhi iguqule indlela amaseli akhe ngayo amaprotheni. Lawa ma-molecule ashintsha i-enzyme esetshenziswa amaseli omdlavuza wesibindi isuka ohlotsheni olulodwa lwe-pyruvate kinase protein (PKM2), evame ukuvezwa kumaseli e-embryonic kanye nomdlavuza, iye kolunye uhlobo lweprotein ye-pyruvate kinase (PKM1), ethuthukisa ukuziphatha kokucindezela isimila. Ukushintsha ukusebenza kwaleli phrotheni kuthinta indlela amangqamuzana omdlavuza asebenzisa ngayo imisoco, okunganciphisa ukukhula kwawo. Njengoba u-Krainer echaza, “Okuhlukile ngendlela yethu ukuthi senza izinto ezimbili ngesikhathi esisodwa: senqaba i-PKM2 futhi sandisa i-PKM1. Futhi sicabanga ukuthi zombili lezi zibalulekile. ”
Ama-ASO ayathembisa ngalolu hlobo lomdlavuza ngoba ngemuva kokuwajova ngaphansi kwesikhumba, umzimba ubuwathumela ngqo esibindini. Umdlavuza wesibindi ubungavinjelwa ukuba ungakhuli futhi usabalale kwezinye izitho. Abacwaningi babone ukuncipha okukhulu ekuthuthukisweni kwezimila kumamodeli amabili wamagundane abawafundile. Lolu cwaningo lwakhela ocwaningweni lwangaphambili elebhu ka-Krainer lapho abashintshe khona i-PKM2 kuya ku-PKM1 kumaseli akhulisiwe besuka ohlotsheni olunolaka lomdlavuza wobuchopho olubizwa ngokuthi i-glioblastoma.
Leli su liphinde libe nenye inzuzo, njengoba amangqamuzana esibindi anempilo engawenzi i-RNA efanayo nama-ASO ayengaqondisa ngayo kumaseli omdlavuza wesibindi. Lokho kunciphisa amathuba okuba khona kwanoma yimiphi imiphumela engeyona eqondiwe. UVoss uthi, "Ukwazi ukuletha lokhu kwelashwa ngqo esibindini, ngaphandle kokuba nomthelela kumaseli ajwayelekile esibindi, kunganikeza indlela ephumelela kakhudlwana, ephephile yokwelapha umdlavuza wesibindi esikhathini esizayo."
UKrainer, osebenza ne-antisense oligonucleotides kwezinye izifo ezihlanganisa i-cystic fibrosis kanye ne-spinal muscular atrophy, uhlela ukuqhubeka nokusebenzisa la mathuluzi okwelapha ukuze afune izindlela zokwelapha umdlavuza wesibindi. Phakathi kweminye imibuzo, abacwaningi banethemba lokuhlola ukuthi ama-molecule e-RNA angasiza yini ukuqukatha ama-metastases omdlavuza esibindini avela kwezinye izitho.
LOKHO ONGAKUTHATHE KULESI SIHLOKO:
- These molecules switch the enzyme that liver cancer cells use from one type of pyruvate kinase protein (PKM2), which is normally expressed in embryonic and cancer cells, to another form of pyruvate kinase protein (PKM1), which enhances tumor-suppressing behavior.
- This study builds on earlier research in Krainer’s lab in which they switched PKM2 to PKM1 in cultured cells from an aggressive type of brain cancer called glioblastoma.
- Among other questions, the researchers hope to explore whether the RNA molecules can help contain the metastases of cancer to the liver from other organs.
