BCL2 expression

This review is an attempt to elaborate molecular targets of luteolin and its role in modulating irregularities in cellular pathways to overcome severe outcomes during diseases including cancer, cardiovascular disorders, diabetes, obesity, inflammation, Alzheimer's disease, Parkinson's disease, hepatic disorders, renal disorders, brain injury, and asthma. As luteolin has enormous therapeutic benefits, it could be a potential candidate in future drug development strategies.

Bax and P21 protein levels were significantly upregulated following DNC treatment, whereas Bcl-2 and P53 protein levels were downregulated in DNC-treated breast cancer cells. In summary, dendrosomal nanocurcumin demonstrated potent anti-tumor effects against breast cancer cells, suggesting its potential as a therapeutic agent in breast cancer treatment.

In this work, we utilized the RNA-sequencing (RNA-seq) technology to analyze the gene expression profiles of primary and recurrent tumor samples from BCa patients received the postoperative standard chemotherapy with doxorubicin (DOX), and identified glutathione S-transferase P1 (GSTP1) as a key factor in regulating chemoresistance. Molecular mechanistic studies revealed that high GSTP1 expression could not only impair the cytotoxicity of DOX by catalyzing the conjugation of reductive glutathione (GSH) with DOX, but also block the c-Jun NH2-terminal kinase (JNK) pathway to promote the proliferation via up-regulating anti-apoptotic B-cell lymphoma-2 (Bcl-2) expression. Given the severe side effects of DOX and the potential of RNA interference (RNAi) technology to silence target gene expression, we developed an endosomal pH-responsive nanoparticle (NP) platform for systemic co-delivery of DOX and GSTP1 siRNA (siGSTP1), and demonstrated its efficacy in reversing chemoresistance and suppressing the growth of DOX-resistant BCa tumors.

Surprisingly, BG11 significantly inhibited tumor proliferation in the MDA-MB-231 xenograft model without obvious toxicity. Based on the above findings, BG11 may be the candidate dual ferroptosis and apoptosis inducers for treating TNBC.

It also restored the cardiac Sirt1/Nrf2/HO-1 signaling pathway. In conclusion, TAX showed significant cardioprotective effects on 5-FU-induced cardiac injury and might represent a promising adjuvant in preventing cardiac injury associated with oxidative stress and inflammation.

Additionally, GADD45a and p21, involved in growth arrest and DNA damage, were significantly upregulated. In conclusion, citalopram's ability to induce apoptosis and alter cell cycle suggests its potential in breast cancer treatment.

MiR-490-3p upregulation inhibited cell proliferation and metastasis but promoted the cell apoptosis and cell-cycle arrest in osteosarcoma via the regulation of CDCA8/ATF3 by targeting NUSAP1. Thus, miR-490-3p might be a potential therapeutic target for the treatment of osteosarcoma.

As a results showed that NP and DX suppressed the proliferation of neuroblastoma cells and could do this through apoptotic pathways. NP can be used to suppress metastasis of SHSY-5Y cells as an inhibitor of the apoptosis pathway Bcl-2. It is thought that NP, which provides tumor suppression through an apoptotic mechanism, may be an alternative treatment agent in neurological cancers such as neuroblastoma.

The cytotoxic effect of engineered T-cells was tested against Rituximab-resistant DLBCL cells (RR-NU-DUL-1)...These findings suggest that CAR T-cell therapy holds great promise for treating refractory DLBCL, offering a potential path for clinical application. This in vitro evaluation highlights the potential of WEE1-engineered T-cells as a targeted treatment strategy for refractory DLBCL, emphasizing their clinical applicability and ability to overcome resistance mechanisms in this aggressive lymphoma subtype.

The combination of KW2478 and cisplatin inhibits colorectal cancer cell proliferation and induces apoptosis by regulating the PI3K/AKT/mTOR pathway.

Our findings demonstrate the therapeutic potential of FAELNs in UC management, highlighting their scalability for mass production and encouraging prospects for clinical transformation.

In contrast, co-treatment with resveratrol significantly reduced these parameters, suggesting its protective effects against CP-induced liver toxicity. We conclude that giving resveratrol can attenuate apoptosis, oxidative stress, inflammation, and histological alterations in the liver induced by CP toxicity.