CCND1 expression

Future research should focus on developing strategies to restore their expression and function, including epigenetic therapies, gene therapy, and small molecule inhibitors. Such approaches could significantly enhance the efficacy of existing treatments and improve patient outcomes.

In vivo studies further demonstrated that cyclobrachycoumarin effectively reduced tumor growth in HT-29 xenograft models by promoting apoptosis and cell cycle arrest, with a favorable tolerability profile. In summary, this study suggests that cyclobrachycoumarin may be a promising candidate for safe and effective CRC therapy.

These results suggest that pterostilbene may offer neuroprotective advantages for differentiated neuronal-like cells. However, further studies are required to confirm these effects in vivo by examining specific biomarkers in human populations consuming pterostilbene-containing foods.

PDT represents a powerful and versatile treatment option for various dermatological conditions due to its ability to target cellular pathways involved in proliferation and apoptosis. Further research into optimizing treatment parameters and combining PDT with other targeted therapies may enhance patient outcomes, reduce resistance, and pave the way for more individualized therapeutic approaches in dermatology.

The potential targets and molecular mechanisms of THSWD in the treatment of NSCLC were preliminarily revealed by a comprehensive analysis in this study, which will provide new ideas and methods for the study of the mechanism of traditional Chinese medicine in treating lung cancer.

CDK4/6 inhibitors such as palbociclib block cell cycle progression and improve outcomes for many ER+/HER2- breast cancer patients...Understanding the molecular mechanisms that allow treated tumor cells to evade arrest is critical for identifying targets of future therapies. Ultimately, we seek to further SPCA as a tool of precision medicine, targeting treatments by individual tumors, and extending this computational framework to interpret other cyclical biological processes represented by high-dimensional data.

P2, N=360, Active, not recruiting, ECOG-ACRIN Cancer Research Group | Trial completion date: Mar 2025 --> Dec 2025 | Trial primary completion date: Dec 2024 --> Dec 2025

Additionally, BNL reduced interleukin-6, JAK1, and STAT3 phosphorylation ((P<0.05) in PC-3 cells that obstructing the expression of proliferation and anti-apoptotic proteins in PC-3 cells. Thus, BNL may be a therapeutic agent against prostate cancer by blocking the STAT3 signaling axis.

Our results suggest the overexpression of CDDN1 is a potentially useful but poor prognostic biomarker for PCa cases.

We identified for the first time that nibmolide treatment to HCC mice significantly attenuated hepatic miRNAs 21 & 221 expressions and sheltered miR-145 expression. These findings were further confirmed with in-silico studies. Moreover, nibmolide treatment in HCC mice regulates miRNA target genes involved in cancer cell proliferation and inflammation, thereby attenuating HCC progression in mice.

Sevo stimulated APC m5C modification and curbed its expression by up-regulating TRDMT1, which in turn activated the β-catenin pathway to stimulate OC cell cycle, invasion, proliferation, and migration and to suppress apoptosis.

The FBXL16 protein expression in Ishikawa/MPA-R cells was significantly higher compared with Ishikawa cells, and the mRNA and protein expression levels of FBXL16 were markedly elevated in the PPVII + miR-33a-5p inhibitor group compared with the PPVII + NC group (P<0.01). These findings suggested that PPVII upregulated the expression of miR-33a-5p, enhanced the sensitivity of EC cells to MPA and potentially exerted anticancer effects in EC through the synergistic action of the miR-33a-5p/FBXL16 axis in combination with MPA.

EGFR and SMAD4 expression were found to be negatively correlated in GBC tissue samples. ERBB2 overexpression/amplification was observed in 30% of the GBC samples. We also found a low percentage of GBC samples to show KRAS codon 12 mutation in Indian GBC patient population, as had been previously documented in pancreatic cancers.

lncRNA MALAT1 is downregulated in meningiomas and associated with increased aggressiveness. Overexpressed cyclin D1 and decreased E-cadherin expression are also associated with high grade meningioma.

Cisplatin resistance is an important cause of bladder cancer relapse...We also demonstrated that E2F8 knockdown suppressed bladder cancer progression in vivo. In conclusion, we verify that E2F8 functioned in bladder cancer, and might exert its function via MCM7.

The results of this study suggest that the expression of IL13Rα2 might be used as a potential prognostic indicator in osteosarcoma patients. Furthermore, it is observed that IL13Rα2 influences the resistance to the chemotherapeutic agent doxorubicin. Therefore, a therapeutic trial targeting IL13Rα2 might be a new therapeutic strategy for osteosarcoma, especially those highly expressing IL13Rα2.

In ex vivo cultured spontaneous MBs, the expression levels of these genes increase after irradiation in CD1 mice, but not in mice with a C57Bl/6 genetic background, suggesting that this signature could predict tumor response to radiation therapy and help develop strategies for targeting DNA damage repair in tumors. A detailed understanding of the mechanisms behind genetic background-related susceptibility to radiation-induced oncogenic responses is crucial for translational research.

More importantly, we found that GH restricted cell proliferation and apoptosis, and inhibited the replication of ALV-J by activating the PI3K/Akt signaling pathway in DF-1 cells. In conclusion, these results indicate GH plays a role in the antiviral response against the replication of ALV-J, providing evidence of an interaction between GH and the innate immunity in chickens.

ZGP protects ovarian function in CTX-induced ovarian aging rats by regulating the Notch1/Nrf2 pathway. It restores serum sex hormone levels, maintains normal follicle development, promotes the proliferation of aged OSCs, optimizes the cell cycle, reduces apoptosis, and preserves stemness, thereby alleviating ovarian aging.

In addition, CA induces apoptosis by enhancing the expression of Bax and caspase-3; and decreased expression of Bcl-2 in prostate cancer cells. Thus, CA might act as a therapeutical application against prostate cancer by targeting the IL-6/JAK/STAT3 signaling axis.

Comprehensive Cyclin D1 quantification, especially above a threshold, significantly correlates with better overall survival in MCL. This highlights its prognostic importance in MCL management. Full quantification of CyclinD1 aids MCL prognosis, while QDB technology for biomarker quantification supports precise clinical prognostic stratification.

Moreover, 4a increased reactive oxygen species (ROS) levels in KYSE 30 cells and upregulated the expression of proteins related to the ROS related MAPK signaling pathway (p-ERK, p-p38, and p-JNK). These findings suggest that compound 4a holds promising potential as an antiproliferative agent by targeting MAPK signaling pathway to inhibit cell cycle progress, induce apoptosis and produce ROS in cancers.

In conclusion, our data show that C1GALT1 enhances the progression of glioma by regulated the O-glycosylation and phosphorylation of EGFR and the subsequent downstream AKT/ERK signaling pathway. Therefore, C1GALT1 represents a potential target for the diagnosis and treatment of glioma.

Co-treatment with SY-5609 and ruxolitinib was synergistically lethal in HEL, SET2 and PD post-MPN-sAML cells.  A CRISPR screen in SET2 and HEL cells revealed BRD4, CBP and p300 as co-dependencies with SY-5609 treatment. Accordingly, co-treatment with SY-5609 and the BETi OTX015 or pelabresib or with the CBP/p300 inhibitor GNE-049 was synergistically lethal in MPN-sAML cells (including those exhibiting TP53 loss). Finally, in the HEL-Luc/GFP xenograft model, compared to each agent alone, co-treatment with SY-5609 and OTX015 reduced post-MPN-sAML burden and improved survival without inducing host toxicity. These findings demonstrate promising preclinical activity of the CDK7i-based combinations with BETi or HATi against advanced-MPNs, including post-MPN-sAML.

Dwon-regulation of ESRP2 inhibited cell proliferation and promoted the sensitivity of chemotherapy drug, Cisplatin(DDP) and Paclitaxel (TAXOL), in MCF-7 cells.Additionally, ESRP2 knockdown obstructed the cell cycle at the G1 phase and caused a decrease in cyclinD1 protein expression. ESRP2 knockdown can inhibit MCF-7 cell proliferation by arresting the cell cycle at the G1 phase and promoting the sensitivity of chemotherapy drugs (DDP and TAXOL)in MCF-7 cells. ESRP2 may be required for the regulation of breast cancer progression, as well as a critical target for the clinical treatment of breast cancer.

Moreover, our analysis of clinical samples shows that the expression of METTL14, USP22, and ERα is upregulated and correlated in BCa tissues. Overall, our findings reveal the key role of the METTL14-USP22-ERα axis in BCa progression, which further provides a druggable target to treat BCa.

Further studies are warranted to validate these findings and explore their clinical implications. Integrating these biomarkers into clinical practice may enhance risk stratification and treatment decisions, ultimately improving outcomes for IBC patients.

Knockdown (KD) of LOXL1 decreased cell proliferation and led to G1 phase arrest in gastric cells. According to GSEA analysis that LOXL1 was positively correlated with the WNT signaling pathway, in vitro experiment proved that LOXL1-KD reduced the phosphorylation level of β-catenin and the expression of the downstream G1 phase checkpoint CCND1.In Conclusion, LOXL1 has been identified as a potential risk prognostic biomarker for gastric cancer by promoting gastric cancer proliferation via WNT/β-catenin/cyclinD1 pathway.

These effects were similarly observed in OC mouse models treated with Tasquinimod. In conclusion, Tasquinimod can improve OC cells' sensitivity to DDP by down-regulating the HDAC4/p21 axis, offering insights into potential strategies for overcoming cisplatin resistance in OC.

Notably, overexpression of PLEKHA4 activated Wnt/β‑catenin signaling, reinforcing its role in promoting β‑catenin nuclear translocation and signaling activity. The present findings suggested that PLEKHA4 could serve as a potential therapeutic target for KIRC; inhibiting PLEKHA4 or modulating Wnt/β‑catenin signaling could provide new avenues for treatment strategies in KIRC.

These findings indicate that miR-545-3p could target and positively correlate with SLC7A11 expression. Additionally, LINC01094 could promote GC cell progression and affect cellular ferroptosis by regulating the miR-545-3p/SLC7A11 signaling axis.

Therefore, melanoma tumor development was prevented by the overexpression of cell cycle inhibitors p16, p21, p27, and p53 due to UM + LunLip treatments. Since the topical application was effective, less invasive, and more practical for the user, this application will be recommended for future steps in in vivo studies.

The combination of Panobinostat with Doxorubicin or Etoposide, both of which are used as standard of care in upfront treatment, leads to a synergistic effect in EWS cells. Overall, our data indicate that HDAC2 is overexpressed in many EWS tumor samples and HDAC inhibition is effective in targeting EWS cells, alone and in combination with standard-of-care chemotherapy agents. This work suggests that the addition of an HDAC inhibitor to upfront treatment may improve response.

As p-HSP27 plays different roles in different stages of nasopharyngeal carcinoma metastasis, it can increase the migration ability of CNE2 cells and reduce its invasion ability. p-HSP27 may induce EMT changes in CNE2 by down-regulating E-cadherin, thus promoting CNE2 migration, and may inhibit CNE2 invasion by down-regulating MMPs expression.

No abstract available

With an increase in FGF6 expression in nude mice, the expression of FGFR4, pERK, Cyclin D1, pAKT, BCL2, GPX4, and ACSL4 increased, and the expression of Caspase9 decreased. FGF6 may change the expression of apoptosis-related proteins and proliferation factors by binding to FGFR4 in the PI3K-AKT/MAPK pathway and may inhibit the ferroptosis of OSCC, thereby possibly participating in the process of inhibiting OSCC.

This study preliminarily explored the involvement of HPRT1 in NPC based on some cellular assays in vitro, which may provide evidence for investigating the specific mechanism underlying the effects of HPRT1 in cancers.

MSC-CM represents a novel therapeutic approach for patients with MASLD requiring PHx.

More investigations might be required to test the mechanistic pathways by which O. ficus-indica (L.) Mill. might exhibit its biological activities in vivo.

Mechanistically, STAT3 emerged as a downstream target gene of GdX. GdX exerts its inhibitory effects on the initiation and progression of BC by negatively modulating the phosphorylation of STAT3.

Furthermore, among the MIA compounds lyaloside and 5(S)-5 carbomethoxy strictosidine had low cytotoxicity and regulated cancer-related signaling, including cell migration, cell invasion, epithelial-mesenchymal transition and immune evasion. Our findings demonstrated that the MIAs used in this study have potential anti-metastasis properties that occur via MMP9-mediated regulation of cancer signaling and have the potential to be used therapeutically at safe doses.

These findings strongly suggest that vinpocetine holds promise as a hepatoprotective agent by targeting a range of oncogenic proteins simultaneously. However, further approaches are needed to validate and establish causal links between our observed effects allowing for a more in-depth exploration of the mechanisms underlying vinpocetine's effects and identifying pivotal determinants of outcomes.