ArticleOncogene2017
Pathobiological implications of the d16HER2 splice variant for stemness and aggressiveness of HER2-positive breast cancer.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed.
- KDM6A alternative splicing induced by 25(OH)D inhibits breast cancer cell stemness through repressing TRAP1 transcription.Oncogene · 2026Article
- Targeting PCSK9, through an innovative cVLP-based vaccine, enhanced the therapeutic activity of a cVLP-HER2 vaccine in a preclinical model of HER2-positive mammary carcinoma.Journal of translational medicine · 2025Article
- CD36 enrichment in HER2-positive mesenchymal stem cells drives therapy refractoriness in breast cancer.Journal of experimental & clinical cancer research : CR · 2025Article
- HER2-Positive Breast Cancer Treatment and Resistance.Advances in experimental medicine and biology · 2025Review
- Expression of c-erb-B2 oncoprotein as a neoantigen strategy to repurpose anti-neu antibody therapy in a model of melanoma.Scientific reports · 2024Article
- Review
- Expression of c-erb-B2 oncoprotein as a neoantigen strategy to repurpose anti-neu antibody therapy in a model of melanoma.Research square · 2024Article
- Loss of the extracellular matrix glycoprotein EMILIN1 accelerates Δ16HER2-driven breast cancer initiation in mice.NPJ breast cancer · 2024Article
- Fatty acid synthase as a new therapeutic target for HER2-positive gastric cancer.Cellular oncology (Dordrecht, Netherlands) · 2023Article
- Preclinical and Basic Research Strategies for Overcoming Resistance to Targeted Therapies in HER2-Positive Breast Cancer.Cancers · 2023Review
- N6-methyladenosine regulated FGFR4 attenuates ferroptotic cell death in recalcitrant HER2-positive breast cancer.Nature communications · 2022Article
- BCL6 and the Notch pathway: a signaling axis leading to a novel druggable biotarget in triple negative breast cancer.Cellular oncology (Dordrecht, Netherlands) · 2022Article
- ERBB2D16 Expression in HER2 Positive Gastric Cancer Is Associated With Resistance to Trastuzumab.Frontiers in oncology · 2022Article
- Trastuzumab resistance in HER2-positive breast cancer: Mechanisms, emerging biomarkers and targeting agents.Frontiers in oncology · 2022Review
- Investigation of the prevalence and clinical implications ofFrontiers in oncology · 2022Article
- Review
- Alternative RNA splicing in stem cells and cancer stem cells: Importance of transcript-based expression analysis.World journal of stem cells · 2021Review
- HER2-PI9 and HER2-I12: two novel and functionally active splice variants of the oncogene HER2 in breast cancer.Journal of cancer research and clinical oncology · 2021Article
- HER2 Isoforms Uniquely Program Intratumor Heterogeneity and Predetermine Breast Cancer Trajectories During the Occult Tumorigenic Phase.Molecular cancer research : MCR · 2021Article
- Review
Corrections and comments
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have previously shown that the d16HER2 splice variant is linked to HER2-positive breast cancer (BC) tumorigenesis, progression and response to Trastuzumab. However, the mechanisms by which d16HER2 contributes to HER2-driven aggressiveness and targeted therapy susceptibility remain uncertain. Here, we report that the d16HER2-positive mammary tumor cell lines MI6 and MI7, derived from spontaneous lesions of d16HER2 transgenic (tg) mice and resembling the aggressive features of primary lesions, are enriched in the expression of Wnt, Notch and epithelial-mesenchymal transition pathways related genes compared with full-length wild-type (WT) HER2-positive cells (WTHER2_1 and WTHER2_2) derived from spontaneous tumors arising in WTHER2 tg mice. MI6 cells exhibited increased resistance to anoikis and significantly higher mammosphere-forming efficiency (MFE) and self-renewal capability than the WTHER2-positive counterpart. Furthermore, d16HER2-positive tumor cells expressed a higher fraction of CD29
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