CCNL1 (Cyclin L1)

CCNL1 overexpression affects breast cancer cells' paclitaxel sensitivity through the PI3K/AKT pathway. CCNL1 activates the NF-κB signaling pathway through its interaction with DVL3; additionally, it promotes the PI3K/AKT pathway. Together, these two mechanisms enable CCNL1 to exert a regulatory role in the progression of breast cancer.

In conclusion, this study reveals a novel mechanism by which lidocaine inhibits HER2-positive breast cancer cell proliferation by targeting the OGT-CCNL1 axis, highlighting a potential therapeutic avenue for HER2-positive breast cancer.

Driver coefficients for TP53INP1, CA12, and CCNL1 aligned with known biology, and epithelial drivers exerted measurable influence on NK cells, consistent with their stage-wise decline. By leveraging temporal single-cell structure, CancerTrace transcends the static and cohort-dependent limitations of existing tools, inferring causal, time-directed driver-modulator relationships that advance mechanistic understanding and precision oncology.

Overexpression of miR-199b-5p promotes proliferation, migration, and EMT in lung cancer cells by targeting CCNL1, with its downstream regulatory effects mediated through the Wnt/β-catenin signaling.

Furthermore, PecA exhibits high efficacy against anaplastic large T cell lymphoma in vitro and in vivo, especially those with constitutively activated STAT3 or STAT3Y640F. In summary, our study describes a distinct and effective di-covalent modification for the dimeric compound PecA to disrupt STAT3 function.

The PI3K/AKT-mTOR pathway is involved in CCNL1-mediated ADM resistance in OS. In summary, CCNL1 is involved in the progression of ADM resistance and OS through the PI3K/AKT-mTOR pathway, which will provide a new clue to the mechanism of ADM resistance and a potential target for the treatment of ADM-resistant OS.

Furthermore, we demonstrate that SAP30BP facilitates CDK11 kinase activities in vitro and in vivo, through ensuring the stabilities and the assembly of cyclins L1/L2 with CDK11. Together, these findings uncover SAP30BP as a critical CDK11 activator that regulates global pre-mRNA splicing.

The Kyoto Encyclopedia of Genes and Genomes pathway enrichment results revealed that the signaling pathways mainly enriched were transcriptional misregulation in cancer, spliceosome, and the IL-17 signaling pathway. Our work identifies a six DNA methylated expression signature as a promising biomarker of chemo-resistance in GC, which provides new insights into the development of new strategies to overcome chemo-resistance in GC.

Expressing mRNA profile data sets GSE98767, GSE45216, and GSE84758 were acquired from the GEO database...The PDT treatment suppressed the G1 to G2/M phase in JNK overexpressed A431 cells. CCNL1, DNAJB1, DUSP6, and EFNB2 were identified as potential PDT target genes in cSCC treatment, whose potential therapeutic mechanism was inhibiting the MAPK pathway and inducing cell cycle alternation.