Oncology Research Editorial Office Published:23 March 2026 The published article titled“MicroRNA 125a-5p Inhibits Cell Proliferation and Induces Apoptosis in Hepatitis B Virus-Related Hepatocellular Carcinoma by Down...Oncology Research Editorial Office Published:23 March 2026 The published article titled“MicroRNA 125a-5p Inhibits Cell Proliferation and Induces Apoptosis in Hepatitis B Virus-Related Hepatocellular Carcinoma by Downregulation of ErbB3”has been retracted from Oncology Research,Vol.27,No.4,2019,pp.449-458.DOI:10.3727/096504017X15016337254623 URL:https://www.techscience.com/or/v27n4/48558.展开更多
Objective:The luminal androgen receptor(LAR)subtype of triple-negative breast cancer(TNBC)differentiation displays low proliferation yet strong metastatic potential and a poor chemotherapy response.This study aimed to...Objective:The luminal androgen receptor(LAR)subtype of triple-negative breast cancer(TNBC)differentiation displays low proliferation yet strong metastatic potential and a poor chemotherapy response.This study aimed to define the molecular basis of the LAR subtype and identify actionable therapeutic targets.Methods:Comprehensive multi-omic analyses were performed on the FUSCC-TNBC cohort,integrating whole-exome sequencing,RNA sequencing,and functional validation in vitro and in vivo.Somatic mutation profiling,gene set enrichment analysis(GSEA),and weighted gene co-expression network analysis(WGCNA)were used to define genomic and transcriptomic signatures.A machine learning model using the Mime1 package was applied to derive a senescence-associated prognostic signature(LAR-S)and validation in external cohorts.Immune deconvolution was performed to decipher the tumor microenvironment.Functional assays,patient-derived organoids(PDOs),and TS/V mouse models were used to evaluate therapeutic responses to senescence-modulating agent and immunotherapy combinations.Results:The LAR subtype was enriched for PIK3CA,PTEN,and ERBB2 kinase domain mutations.Functional studies confirmed ERBB2 variants(e.g.,V777L and E698_P699delinsA)as oncogenic drivers conferring sensitivity to neratinib.Transcriptomic analyses revealed a dominant cellular senescence program associated with immune suppression.The LAR-S signature stratified survival across cohorts and predicted immunotherapy resistance.Targeting cellular senescence inhibited LAR subtype organoid growth and when combined with anti-PD-1 therapy synergistically suppressed tumor growth in vivo.Conclusions:The LAR subtype harbors two therapeutic vulnerabilities:ERBB2 mutation-driven kinase activation;and senescencemediated immune evasion.The LAR-S signature enables precise patient stratification and supports senescence-targeted and immunotherapy combination strategies as promising approaches for this refractory TNBC subtype.展开更多
The ErbB signaling network has recently emerged as a key modulator of central nervous system responses to injury.This review provides a comprehensive overview of ErbB receptors and their ligands,highlighting canonical...The ErbB signaling network has recently emerged as a key modulator of central nervous system responses to injury.This review provides a comprehensive overview of ErbB receptors and their ligands,highlighting canonical and non-canonical signaling mechanisms relevant to brain damage.We explore how ErbB signaling is dynamically regulated following injury and how it orchestrates processes such as neuroinflammation,gliosis,and neural repair.Special attention is given to its interplay with other critical pathways,including Notch signaling,and its roles within adult neurogenic niches,where it modulates neural stem cell behavior in response to damage.Based on accumulating preclinical evidence,we propose two therapeutic strategies for targeting ErbB signaling in brain injury:(1)dampening neuroinflammation through ErbB inhibition and(2)promoting neuroprotection and neurogenesis via neuregulin-1-mediated activation.The first strategy is supported by studies,which demonstrate that inhibition of ErbB1 limits neuroinflammation and supports neural repair in preclinical models.The latter strategy is supported by emerging studies demonstrating the significant potential of novel protein kinase C activating diterpenes in modulating ErbB signaling pathways through the regulation of neuregulin-1 release.Diterpenes,by influencing the ErbB pathway,may uniquely bridge the gap between neuroprotection and regeneration.Their potential to modulate inflammation and promote pro-regenerative cellular environments positions them as promising tools in the development of targeted therapies.By dissecting these mechanisms,we aim to shed light on the translational potential of ErbB-targeted therapies and their capacity to enhance endogenous repair processes in the injured brain.展开更多
文摘Oncology Research Editorial Office Published:23 March 2026 The published article titled“MicroRNA 125a-5p Inhibits Cell Proliferation and Induces Apoptosis in Hepatitis B Virus-Related Hepatocellular Carcinoma by Downregulation of ErbB3”has been retracted from Oncology Research,Vol.27,No.4,2019,pp.449-458.DOI:10.3727/096504017X15016337254623 URL:https://www.techscience.com/or/v27n4/48558.
基金funding from the Ministry of Science and Technology of China(Grant Nos.2023YFF1205003,2023YFF0613304,and 2023YFC3402504)the National Key R&D Program of China(Grant No.2023YFF0613300,2023YFF1205003)the National Natural Science Foundation of China(Grant Nos.82473499,82272957,and 82303735).
文摘Objective:The luminal androgen receptor(LAR)subtype of triple-negative breast cancer(TNBC)differentiation displays low proliferation yet strong metastatic potential and a poor chemotherapy response.This study aimed to define the molecular basis of the LAR subtype and identify actionable therapeutic targets.Methods:Comprehensive multi-omic analyses were performed on the FUSCC-TNBC cohort,integrating whole-exome sequencing,RNA sequencing,and functional validation in vitro and in vivo.Somatic mutation profiling,gene set enrichment analysis(GSEA),and weighted gene co-expression network analysis(WGCNA)were used to define genomic and transcriptomic signatures.A machine learning model using the Mime1 package was applied to derive a senescence-associated prognostic signature(LAR-S)and validation in external cohorts.Immune deconvolution was performed to decipher the tumor microenvironment.Functional assays,patient-derived organoids(PDOs),and TS/V mouse models were used to evaluate therapeutic responses to senescence-modulating agent and immunotherapy combinations.Results:The LAR subtype was enriched for PIK3CA,PTEN,and ERBB2 kinase domain mutations.Functional studies confirmed ERBB2 variants(e.g.,V777L and E698_P699delinsA)as oncogenic drivers conferring sensitivity to neratinib.Transcriptomic analyses revealed a dominant cellular senescence program associated with immune suppression.The LAR-S signature stratified survival across cohorts and predicted immunotherapy resistance.Targeting cellular senescence inhibited LAR subtype organoid growth and when combined with anti-PD-1 therapy synergistically suppressed tumor growth in vivo.Conclusions:The LAR subtype harbors two therapeutic vulnerabilities:ERBB2 mutation-driven kinase activation;and senescencemediated immune evasion.The LAR-S signature enables precise patient stratification and supports senescence-targeted and immunotherapy combination strategies as promising approaches for this refractory TNBC subtype.
基金supported by the I+D+i(PID2022-142418OB-C21)grant funded by MICIU/AEI/10.13039/501100011033 and by ERDF/UE.
文摘The ErbB signaling network has recently emerged as a key modulator of central nervous system responses to injury.This review provides a comprehensive overview of ErbB receptors and their ligands,highlighting canonical and non-canonical signaling mechanisms relevant to brain damage.We explore how ErbB signaling is dynamically regulated following injury and how it orchestrates processes such as neuroinflammation,gliosis,and neural repair.Special attention is given to its interplay with other critical pathways,including Notch signaling,and its roles within adult neurogenic niches,where it modulates neural stem cell behavior in response to damage.Based on accumulating preclinical evidence,we propose two therapeutic strategies for targeting ErbB signaling in brain injury:(1)dampening neuroinflammation through ErbB inhibition and(2)promoting neuroprotection and neurogenesis via neuregulin-1-mediated activation.The first strategy is supported by studies,which demonstrate that inhibition of ErbB1 limits neuroinflammation and supports neural repair in preclinical models.The latter strategy is supported by emerging studies demonstrating the significant potential of novel protein kinase C activating diterpenes in modulating ErbB signaling pathways through the regulation of neuregulin-1 release.Diterpenes,by influencing the ErbB pathway,may uniquely bridge the gap between neuroprotection and regeneration.Their potential to modulate inflammation and promote pro-regenerative cellular environments positions them as promising tools in the development of targeted therapies.By dissecting these mechanisms,we aim to shed light on the translational potential of ErbB-targeted therapies and their capacity to enhance endogenous repair processes in the injured brain.
