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The Catholic University of Korea

Research Results


Catholic University Professor Yong-Yeon Cho's Team Identifies World's First Killing Mechanism of 'Re

  • Writer :External Affairs Team
  • Date :2026.09.04
  • Views :37

  • - World's First Verification of Anticancer Efficacy of Novel Apoptosis Pathway 'Carryoptosis' Independently Identified by Domestic Researchers
  • - Published in 'Journal of Pharmaceutical Analysis' (IF 11.2, Top 4.1%), the World's Most Prestigious Journal in the Pharmacy Field


Photo caption: (From left) Professor Yong-Yeon Cho (Corresponding Author), College of Pharmacy, Catholic University of Korea; Researcher Ji-In Byun (First Author / Currently a Ph.D. student at the University of Washington)


 A research team led by Professor Yong-Yeon Cho of the College of Pharmacy at the Catholic University of Korea (President Jun-Kyu Choi) has identified a new cell death mechanism that can effectively control malignant cancer cells that were difficult to treat due to resistance to existing anticancer drugs.


 'Anticancer resistance,' which develops from repeated administration of anticancer drugs during cancer treatment, is a major cause of treatment failure and cancer recurrence. Conventional anticancer drugs primarily kill cancer cells by stimulating a cell death pathway called 'apoptosis,' but there was a limitation in that cancer cells that acquired resistance had this pathway blocked, rendering the drugs ineffective. 


 Professor Yong-Yeon Cho's research team applied 'Karyoptosis,' a regulatory cell death mechanism whose mechanism was elucidated for the first time in the world through the independent research capabilities of domestic researchers, to platinum-based anticancer drug-resistant colorectal cancer cells. Karyoptosis is a phenomenon in which a cell dies as its 'nuclear membrane,' a key control mechanism, bursts explosively.


 Figure description: Although cancer cells acquire resistance upon treatment with platinum-based anticancer drugs, the induction of carioptosis induced apoptosis in both platinum-based anticancer drug-sensitive and resistant cell groups without differentiation.


 Experimental results confirmed that when the cleavage transcription factor (CREB3-CF) that induces carioptosis was overexpressed, cancer cell proliferation was suppressed in anticancer drug-resistant colon cancer cells to the same level as in susceptible cells prior to acquiring resistance. This is an independent cell death pathway completely distinct from existing apoptosis, necroptosis, and autophagy, and is the world's first achievement to demonstrate that it can induce cancer cell death regardless of the presence or absence of anticancer drug resistance. 


 This study has established a milestone in the development of new treatments capable of controlling intractable malignant cancers, including metastatic cancer cells, and is expected to serve as a source technology for developing therapeutic agents for various human diseases through the regulation of nuclear membrane integrity.


 Professor Yong-Yeon Cho of the Catholic University College of Pharmacy stated, “This study is highly significant in that it verified that carry-optosis, which was first identified by domestic researchers, can even control the proliferation of anticancer drug-resistant cells,” adding, “We hope that this will be utilized as a source technology for the development of treatments for intractable cancers and various human diseases in the future through the new target of regulating nuclear membrane integrity.” 


 Meanwhile, the results of this study were published online on July 29 in the ‘Journal of Pharmaceutical Analysis’ (2026 IF: 11.2, top 4.1% in the Pharmacology & Pharmacy field), a world-leading academic journal in the field of pharmacy.


 (End) 


Image description




Inhibitory effect of carioptosis induced by CREB3-CF on cancer cell proliferation.


The induction of carioptosis induced by overexpression of CREB3-FL or CREB3-CF in colorectal cancer cell lines was confirmed by cell immunofluorescence (A), and it was confirmed that cancer cell growth was inhibited in both groups by treating platinum-based anticancer drug-sensitive and resistant cells with this (B).