High-throughput screening cell panel is very important tool in drug research and development, the tested sensitive cell lines can provide references for in vivo models or indication for the selection of clinical trial subjects. Cell Panel screening can be used to study the mechanism of action and selectivity of drugs, and combined with bioinformatics studies can help researchers discover biomarkers of drug response. Moreover, Cell Panel screening can be used to study whether combination therapy strategies improve cancer treatment effect and solve clinical drug resistance and other problems.
The Human RAS Oncogenes play a vital role in cancer development, including KRAS, NRAS and HRAS, KRAS is the most frequently mutated RAS isoform with a mutation incidence of >10% across all cancers, and up to 70% and 20% in pancreatic and non-small cell lung cancer (NSCLC), respectively.
Werner Syndrome (WS) is an autosomal-recessive genetic disorder characterized by premature ageing and DNA repair defects because of mutations in the WRN gene. WRN is a RecQ family protein with helicase, strand annealing and exonuclease activities. WRN localizes to the sites of damaged DNA, interacts with several DNA repair pathways including base excision DNA repair, non-homologous end-joining (NHEJ), homologous recombination (HR) and replication re-start after DNA damage.
Here, we constructed an experimental cascade from in vitro to in vivo, which is composed of protein production, biochemical assays, cell line construction, cellular assays, and animal modeling. This WRN screening cascade can satisfy the mechanism study of WRN as well as efficient and comprehensive screen of WRN inhibitor, thus accelerate the novel drug discovery.
A new collaborative report from IARC. There were almost 20 million new cases of cancer and close to 10 million deaths from cancer in 2022. Despite an estimated increase to more than 2.31 million new cases, breast cancer became the second most common cancer type, after lung cancer. The most common subtype, hormone-receptor-positive/HER2-negative (HR+ or ER+/HER2-), accounts for 69% of all cases. Cyclin-dependent kinase (CDK) 4/6 inhibition in combination with endocrine therapy is the standard-of-care treatment for patients with advanced-stage HR+HER2- breast cancer. Cell cycle regulators with promising clinical potential include CDK2, CDK4, CDK7, PLK4, WEE1, PKMYT1, AURKA and TTK. Novel inhibitors of these targets, alone or in combination, may overcome CDK4/6 inhibitor resistance. Based on this, we have established a series of in vivo and in vitro assays on CDK family targets. On this basis, we have established a series of in vitro and in vivo experiments on CDK family targets, which can achieve high-throughput screening in vitro experiments, providing a faster screening strategy for CDKs inhibitors.
The PARP (Poly(ADP-ribose) polymerase) family consists of enzymes vital for cellular functions, notably DNA repair, crucial for genomic stability. Once malfunction, these enzymes can contribute to various diseases, including cancer, neurodegenerative disorders, and inflammatory conditions. PARP inhibitors (PARPi), which target these enzymes, have shown promise as treatments for certain cancers, particularly those with DNA repair pathway defects such as BRCA-mutated cancer. Here, we have developed and validated PARP-related biochemical assays, cell-based assays, drug resistant cell line construction, and in vivo pharmacology models to support novel PARPi discovery.
