Pub Date : 2026-02-07DOI: 10.1186/s12935-026-04199-1
Sheng-Qi Du, Ya-Tong Liu, Fen Yang, Jun Zhang
{"title":"Potential correlation between high SNHG expression and poor pancreatic cancer prognosis: evidence from systematic reviews and meta-analyses.","authors":"Sheng-Qi Du, Ya-Tong Liu, Fen Yang, Jun Zhang","doi":"10.1186/s12935-026-04199-1","DOIUrl":"https://doi.org/10.1186/s12935-026-04199-1","url":null,"abstract":"","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":" ","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146137459","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-06DOI: 10.1186/s12935-026-04210-9
Mao Ye, Bita Badehnoosh
{"title":"The emerging role of TROP2 as a diagnostic and prognostic biomarker in bladder tumor.","authors":"Mao Ye, Bita Badehnoosh","doi":"10.1186/s12935-026-04210-9","DOIUrl":"https://doi.org/10.1186/s12935-026-04210-9","url":null,"abstract":"","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":" ","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146131521","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Chimeric antigen receptor natural killer (CAR-NK) cells represent a promising "off-the-shelf" alternative to CAR-T cells, offering a superior safety profile and inherent multi-antigen targeting capabilities. However, their clinical potential is constrained by the "CRISPR ceiling", a set of practical limitations of DSB-based CRISPR-Cas9 such as DNA double-strand break (DSB)-associated chromosomal rearrangements and p53-mediated fitness loss, low efficiency for safe, large, multicistronic knock-ins, and rigid promoter-driven transgene expression that can cause tonic signaling. Importantly, next-generation, DSB-free base and prime editors reduce or eliminate the DSB-associated genotoxic stress observed with nuclease cutting, CRISPR-associated transposases now enable programmable, targeted insertion strategies that can accommodate larger cassettes, and synthetic/epigenetic circuits provide dynamic, context-dependent transgene control that avoids constitutive promoter-driven tonic signaling. This review explores technological approaches beyond conventional CRISPR, highlighting next-generation precision engineering tools that may enable improved CAR-NK therapies and represent potential advances in safety and efficacy. We detail how base editing, epigenetic reprogramming, targeted transposon systems, and synthetic biology circuits can be synergistically integrated to overcome critical clinical challenges. These advanced technologies enable the precise enhancement of three fundamental pillars of efficacy: Persistence through endogenous cytokine armoring and metabolic engineering; Trafficking via chemokine receptor matching and stromal barrier degradation; and Tumor Eradication using logic-gated targeting, immunomodulatory payloads, and bispecific engagers. By synthesizing these cutting-edge advances, we provide a roadmap for developing next-generation CAR-NK cells capable of durable, potent, and safe antitumor responses against both hematological and solid malignancies, ultimately forging a new frontier in accessible cellular immunotherapy.
{"title":"Beyond CRISPR: next-gen precision engineering of CAR-NK cells for enhanced persistence, trafficking, and tumor eradication.","authors":"Aiyun Dong, Hamed Soleimani Samarkhazan, Farzaneh Tavakoli","doi":"10.1186/s12935-026-04219-0","DOIUrl":"https://doi.org/10.1186/s12935-026-04219-0","url":null,"abstract":"<p><p>Chimeric antigen receptor natural killer (CAR-NK) cells represent a promising \"off-the-shelf\" alternative to CAR-T cells, offering a superior safety profile and inherent multi-antigen targeting capabilities. However, their clinical potential is constrained by the \"CRISPR ceiling\", a set of practical limitations of DSB-based CRISPR-Cas9 such as DNA double-strand break (DSB)-associated chromosomal rearrangements and p53-mediated fitness loss, low efficiency for safe, large, multicistronic knock-ins, and rigid promoter-driven transgene expression that can cause tonic signaling. Importantly, next-generation, DSB-free base and prime editors reduce or eliminate the DSB-associated genotoxic stress observed with nuclease cutting, CRISPR-associated transposases now enable programmable, targeted insertion strategies that can accommodate larger cassettes, and synthetic/epigenetic circuits provide dynamic, context-dependent transgene control that avoids constitutive promoter-driven tonic signaling. This review explores technological approaches beyond conventional CRISPR, highlighting next-generation precision engineering tools that may enable improved CAR-NK therapies and represent potential advances in safety and efficacy. We detail how base editing, epigenetic reprogramming, targeted transposon systems, and synthetic biology circuits can be synergistically integrated to overcome critical clinical challenges. These advanced technologies enable the precise enhancement of three fundamental pillars of efficacy: Persistence through endogenous cytokine armoring and metabolic engineering; Trafficking via chemokine receptor matching and stromal barrier degradation; and Tumor Eradication using logic-gated targeting, immunomodulatory payloads, and bispecific engagers. By synthesizing these cutting-edge advances, we provide a roadmap for developing next-generation CAR-NK cells capable of durable, potent, and safe antitumor responses against both hematological and solid malignancies, ultimately forging a new frontier in accessible cellular immunotherapy.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":" ","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146123939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-05DOI: 10.1186/s12935-026-04214-5
Julia Held, Marc A Schneider, Beatriz Martinez-Delgado, Bin Liu, David S DeLuca, Elena Korenbaum, Sabina Janciauskiene, Thomas Muley
{"title":"Exploring the effects of tinzaparin and cisplatin on lung cancer cells in vitro.","authors":"Julia Held, Marc A Schneider, Beatriz Martinez-Delgado, Bin Liu, David S DeLuca, Elena Korenbaum, Sabina Janciauskiene, Thomas Muley","doi":"10.1186/s12935-026-04214-5","DOIUrl":"https://doi.org/10.1186/s12935-026-04214-5","url":null,"abstract":"","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":" ","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146123199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-04DOI: 10.1186/s12935-026-04218-1
Laura S Hildebrand, Babak Pornour Mehravani, Mohammed Khalifa, Paula Schiller, Janis Langkrär, Tina Jost, Rainer Fietkau, Luitpold V Distel
{"title":"The inhibition of the MRN complex by Mirin radiosensitizes particularly HPV-negative HNSCC cell lines.","authors":"Laura S Hildebrand, Babak Pornour Mehravani, Mohammed Khalifa, Paula Schiller, Janis Langkrär, Tina Jost, Rainer Fietkau, Luitpold V Distel","doi":"10.1186/s12935-026-04218-1","DOIUrl":"https://doi.org/10.1186/s12935-026-04218-1","url":null,"abstract":"","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":" ","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146117980","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-03DOI: 10.1186/s12935-026-04205-6
Zimeng Liu, Changda Yu, Xiong Yu, Bo Shao, Chen Li
Objective: To investigate the significance of DCUN1D5 in colorectal cancer (CRC) progression and determine the underlying mechanism.
Methods: We analyzed DCUN1D5 expression levels in CRC tissues using the TCGA and GEO databases and conducted immunohistochemistry and qPCR in retrieved CRC tissues. shRNA-mediated knockdown of DCUN1D5 in CRC cell lines was performed to investigate its effects on cell growth and motility. In addition, DCUN1D5-mediated promotion of CUL1 neddylation was examined using immunoblotting, the antitumor effects of inhibiting the neddylation pathway was evaluated using the inhibitor MLN4924, and the effects of silencing DCUN1D5 and MLN4924 treatment were validated in vivo using xenograft models.
Results: DCUN1D5 was found to be significantly overexpressed in CRC tissues, and its knockdown impaired CRC cell proliferation and migration, which was associated with reduced CUL1 neddylation. Inhibition of the neddylation pathway using the NEDD8 inhibitor MLN4924 supported these observations. In vivo, DCUN1D5 silencing and MLN4924 treatment led to reduced tumor growth and metastasis.
Conclusion: DCUN1D5 contributes to the growth and motility of CRC in vitro and in vivo.
{"title":"DCUN1D5 promotes the proliferation and migration of colorectal cancer tumors in vitro and in vivo.","authors":"Zimeng Liu, Changda Yu, Xiong Yu, Bo Shao, Chen Li","doi":"10.1186/s12935-026-04205-6","DOIUrl":"https://doi.org/10.1186/s12935-026-04205-6","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the significance of DCUN1D5 in colorectal cancer (CRC) progression and determine the underlying mechanism.</p><p><strong>Methods: </strong>We analyzed DCUN1D5 expression levels in CRC tissues using the TCGA and GEO databases and conducted immunohistochemistry and qPCR in retrieved CRC tissues. shRNA-mediated knockdown of DCUN1D5 in CRC cell lines was performed to investigate its effects on cell growth and motility. In addition, DCUN1D5-mediated promotion of CUL1 neddylation was examined using immunoblotting, the antitumor effects of inhibiting the neddylation pathway was evaluated using the inhibitor MLN4924, and the effects of silencing DCUN1D5 and MLN4924 treatment were validated in vivo using xenograft models.</p><p><strong>Results: </strong>DCUN1D5 was found to be significantly overexpressed in CRC tissues, and its knockdown impaired CRC cell proliferation and migration, which was associated with reduced CUL1 neddylation. Inhibition of the neddylation pathway using the NEDD8 inhibitor MLN4924 supported these observations. In vivo, DCUN1D5 silencing and MLN4924 treatment led to reduced tumor growth and metastasis.</p><p><strong>Conclusion: </strong>DCUN1D5 contributes to the growth and motility of CRC in vitro and in vivo.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":" ","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146112447","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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