CCNE1 overexpression

The downregulation of miR-9-5p significantly reduces the CCNE1 level in A549 cells, and the upregulation of LINC01116 counteracts the downregulation of miR-9-5p effect, restoring the expression level of CCNE1. Our data demonstrated that LINC01116 regulates the expression of CCNE1 by positively regulating miR-9-5p, thereby affecting cell cycle, proliferation and participating in the development of LUAD.

CCNE1 is expected to be a potential biomarker for tumor prognosis and immune infiltration in various cancers.

We reviewed demographic data, treatment histories, and overall response rates (ORR). We identified five patients with DDLPS who were treated with CDK4/6i, palbociclib and abemaciclib. In untreated WD/DD LPS, baseline alterations in cyclin D are rare. Our analysis revealed that three patients with DDLPS acquired either cyclin D1 or cyclin D2 amplification in progressing samples following treatment with CDK4/6i. Unlike breast cancer, where cyclin E1 amplification is a well-established driver of resistance to CDK4/6i, these findings suggest a potential role for cyclin D amplification in acquired resistance in LPS.

Real-world survival analysis demonstrated that patients with CCNE1-amplified gastric cancer had worse survival after trastuzumab for HER2-positive tumors, but better survival after immunotherapy. These data suggest that CCNE1-amplified gastric cancer has a distinct molecular and immune profile with important therapeutic implications, and therefore further investigation of CCNE1 amplification as a predictive biomarker is warranted.

Our data not only identified the prognostic/predictive significance of these key cell cycle regulators but also demonstrate the importance of sub-cellular localisation. CDK2 targeting in cyclin-E1-amplified OCs could be a rational approach.

Finally, analysis of breast cancer samples reveals a positive correlation between Cyclin E1 amplification and RAD52 expression. These findings demonstrate the importance of suppressing mitotic defects in Cyclin E1-overexpressing cells through RAD52.

CircROR1 upregulates CCNE1 expression through KAT2A-mediated histone acetylation. Our research confirms the critical role of CircROR1 in melanoma invasion and metastasis, and CircROR1 could serve as a potential therapeutic target for melanoma treatment.

The ceRNA network and WGCNA analyses are useful to identify novel DEGs that can serve as prognostic markers in cervical cancer. The DEGs will be validated in future studies.

The review extends beyond CDK2i to encompass novel emerging CDK4 inhibitors, combined CDK2/4/6 inhibitors, and the well-known pan-CDK inhibitors including those specifically directed at CDK2. Delving into the results, we critically appraise the observed clinical efficacy and offer valuable insights into their potential impact and future applications.

Thus, C14MC is a tumor-suppressive and methylation-regulated miRNA cluster in CC. Reactivation of C14MC can be useful in the management of CC.

The results of the druggability evaluation showed that III-13 was characterized by low bioavailability and poor membrane permeability when orally administered, suggesting the necessity of further structural modifications. Therefore, this study provided a lead compound for antitumor drugs, especially those against CCNE1-amplified tumor proliferation.

Finally, depletion of FBXL12 exacerbated oncogene-induced replication stress and sensitized cancer cells to drug-induced replication stress by WEE1 inhibition. Collectively, our results indicate that FBXL12 constitutes a vulnerability and a potential therapeutic target in CYCLIN E-overexpressing cancers.