PurposeDYNLT3 is identified as an age‐related gene. Nevertheless, the specific mechanism of its carcinogenesis in breast tumor has not been clarified. This research aims to elucidate the role and the underlying molecular pathways of DYNLT3 on breast cancer tumorigenesis.MethodsThe differential expression of DYNLT3 among breast cancer, breast fibroids, and normal tissues, as well as in various breast cancer cell lines were detected by immunohistochemical staining, real‐time quantitative reverse transcription‐PCR and Western blotting, respectively. Additionally, the role of DYNLT3 on cell viability and proliferation were observed through cell counting kit‐8, bromodeoxyuridine, and colony formation experiments. Migratory and invasive abilities was envaulted by wound healing and Transwell methods. Apoptotic cells rate was examined by flow cytometry. Furthermore, nude mice xenograft models were established to confirm the role of DYNLT3 in tumor formation in vivo.ResultsDYNLT3 expression was highly rising in both breast cancer tissues and cells. DYNLT3 knockdown obviously suppressed cell growth, migration and invasion, and induced cell apoptosis in MDA‐MB‐231 and MCF‐7 breast cancer cells. The overexpression of DYNLT3 exerted the opposite effect in MDA‐MB‐231 cells. Moreover, DYNLT3 knockdown inhibited tumor formation in vivo. Mechanistically, an elevation of N‐cadherin and vimentin levels and a decline of E‐cadherin were observed when DYNLT3 was upregulated, which was reversed when DYNLT3 knockdown was performed.ConclusionDYNLT3 may function as a tumor‐promotor of age‐associated breast cancer, which is expected to provide experimental basis for new treatment options.

Metastasis and paclitaxel (PTX) resistance are the main reason for the poor prognosis of ovarian cancer (OC).Evidence showed that RNA-binding proteins (RBPs) and long noncoding RNAs (lncRNAs) can modulate posttranscriptional regulation. The aim of this study was to determine the relationship among RBP, lncRNA and OC and to further guide clinical therapy. Immunohistochemistry revealed that pre-mRNA processing factor 6 (PRPF6) was upregulated in OC chemoresistant tissues and was closely related to advanced (Federation of International of Gynecologists and Obstetricians) FIGO stages and chemo-resistance. PRPF6 promoted progression, and PTX resistance in vitro and in vivo. And the transcripts of small nucleolar RNA host gene SNHG16-L/S were differentially expressed in OC cells and tissues as detected through real-time PCR (RT-PCR). SNHG16-L/S had opposite effects on progression and PTX resistance in OC. Mechanistically, SNHG16-L inhibited GATA-binding protein 3 (GATA3) transcription by binding to CCAAT/enhancer-binding protein B (CEBPB). Moreover, PRPF6 induced the alternative splicing of SNHG16, causing downregulation of SNHG16-L and, leading to the upregulation of GATA3 expression to further promote metastasis and PTX-resistance in OC. Totally, these data unveiled that PRPF6 promotes metastasis and PTX resistance of OC through SNHG16-L/CEBPB/GATA3 axis, which provides a new direction for OC treatment.