CCNE2 (Cyclin E2)

Therapeutically, OSMR neutralization with vixarelimab synergized with fluorouracil to overcome chemoresistance and reinstate anti-tumor immunity in GC preclinical models. Our findings establish OSMR as a molecular linchpin connecting intrinsic tumor survival pathways (PI3K/CCNE2) with extrinsic immunosuppressive reprogramming (BMP5/TANs/CD8+T cells), providing a clinically actionable target to overcome treatment resistance in GC.

The combination of VEN and CDM exerts synergistic anti-leukemia effects by inhibiting cellular proliferation, inducing G0/G1 phase arrest and promoting apoptosis through PI3K/AKT/FoxO1 axis in T-ALL.

In the present study, the signaling pathways involved in cell cycle regulation were further investigated and it was found that PTPN18 may regulate the expression levels of cyclin‑dependent kinase (CDK) inhibitor 1A and CDK inhibitor 1B proteins through phosphatidylinositol 3‑kinase/protein kinase B signaling pathway, which leads to cell cycle arrest and tumor inhibition in BC. Thus, analysis of the tumor suppressor mechanism of PTPN18 not only helps us to understand its biological function but also provides a theoretical basis for the development of new therapeutic strategies for BC.

Both in vitro cell culture experiments and in vivo models supported ZMIZ2's role in promoting proliferation. ZMIZ2 promotes PCa cell proliferation through the AR signaling pathway by regulating key cell-cycle genes, highlighting it as a potential therapeutic target.

Contrary to the situation in normal development, the results show that either Cyclin E1 or Cyclin E2 is essential for tumorigenesis. They also suggest that in the absence of Cyclin E1, Cyclin E2 serves homeostasis, whereas the oncogenic pathways suppress this compensation as an anti-tumour, self-preserve mechanism.

miR-30a-5p participates in regulating the proliferation of Wilms tumor cells by suppressing the CCNE2/p-Rb/E2F1 axis.

These findings indicate that γT3 and δT3 inhibit HCC2998 cell proliferation by activating the DDR pathway, highlighting their potential as therapeutic agents to overcome cell cycle arrest resistance in CRC. This study provides critical insights into the molecular actions of γT3 and δT3, supporting their further investigation as promising candidates for CRC intervention.

This degradation relieves FOXP1 repression of Cyclin E2, promoting CRC cell proliferation. In summary, FBXO44 is an oncogene that promotes CRC tumorigenesis by degrading FOXP1 and upregulating Cyclin E2, offering a potential therapeutic target for CRC.

In the present study, we analyzed the role of the KMT2D p. (Arg191Trp) variant in imatinib-resistant CML, which was recurrently acquired in imatinib resistance in vitro...Overall, our findings demonstrate that the loss of the tumor suppressor KMT2D promotes TKI resistance in CML. Thus, KMT2D status could serve as an additional biomarker for TKI resistance, while restoration of its expression might be a therapeutic option to overcome this resistance.

(4) Our findings indicate that CE2 expression is upregulated in PH/DEN cells, with a notable decrease in the presence of M1 macrophages. In contrast, compared with control macrophages, M1 macrophages did not significantly affect Mapk4/7 expression.

Knockdown of Angptl4 or Prl8a6 in periwound skin tissue impairs EpSC proliferation and delays wound re-epithelialization. In conclusion, our study demonstrates that, after skin injury, elevated levels of proinflammatory cytokines and growth factors in periwound tissue stimulate Angptl4 expression in EpSCs and that ANGPTL4 promotes EpSC proliferation by increasing Prl8a6 expression, thereby accelerating wound re-epithelialization.

In antitumor activity in vitro, α-caryophyllene exhibited obvious selective cytotoxicity, and its cytotoxicity against lung cancer A549 cells (IC50 = 22.94 ± 0.56) was superior to the elemene injection (EI, positive control), while its toxicity against normal cell lines was lower (MRC-5: IC50 = 76.66 ± 2.60 μg/mL, L929: IC50 = 44.04 ± 0.72 μg/mL)...In antitumor activity in vivo, α-caryophyllene effectively suppressed transplanted tumor growth by inducing apoptosis of transplanted tumor cells and was superior to the positive control EI. Therefore, α-caryophyllene has outstanding anticancer properties in vitro and in vivo, showing great potential to become a new anticancer drug in the pharmaceutical field.