A5015967895- PARP inhibition in cancer therapy
- Ovarian cancer diagnosis and treatment
- Autophagy in Disease and Therapy
- RNA modifications and cancer
- Microtubule and mitosis dynamics
- Cancer-related Molecular Pathways
- Heat shock proteins research
- Cancer Mechanisms and Therapy
- Cancer, Lipids, and Metabolism
- Cancer Research and Treatments
- Peptidase Inhibition and Analysis
- Chronic Lymphocytic Leukemia Research
- Advanced Breast Cancer Therapies
- Cell death mechanisms and regulation
- Cancer-related molecular mechanisms research
- ATP Synthase and ATPases Research
- Ferroptosis and cancer prognosis
- HER2/EGFR in Cancer Research
- Kruppel-like factors research
- NF-κB Signaling Pathways
- Cancer, Hypoxia, and Metabolism
- Monoclonal and Polyclonal Antibodies Research
- Immune Cell Function and Interaction
- Biochemical and Molecular Research
- Histone Deacetylase Inhibitors Research
The University of Texas MD Anderson Cancer Center
2011-2024
Purpose: Salt-inducible kinase 2 (SIK2) is a centrosome required for mitotic spindle formation and potential target ovarian cancer therapy. Here, we examine the effects of novel small-molecule SIK2 inhibitor, ARN-3236, on sensitivity to paclitaxel in cancer.Experimental Design: expression was determined tissue samples cell lines. ARN-3236 tested its efficiency inhibit growth enhance cultures xenografts siRNA were compared their ability produce nuclear-centrosome dissociation, splitting,...
Poly(adenosine diphosphate ribose) polymerase (PARP) inhibitors exhibit promising activity against ovarian cancers, but their efficacy can be limited by acquired drug resistance. This study explores the role of autophagy in regulating sensitivity cancer cells to PARP inhibitors.Induction was detected punctate LC3 fluorescence staining, LC3I LC3II conversion on Western blot analysis, and electron microscopy. Enhanced growth inhibition apoptosis were observed when used with hydroxychloroquine,...
Poly(ADP-ribose) polymerase inhibitors (PARP inhibitors) have had an increasing role in the treatment of ovarian and breast cancers. PARP are selectively active cells with homologous recombination DNA repair deficiency caused by mutations BRCA1/2 other pathway genes. Cancers proficiency respond poorly to inhibitors. that initially eventually develop drug resistance. We identified salt-inducible kinase 2 (SIK2) inhibitors, ARN3236 ARN3261, which decreased double-strand break (DSB) functions...
Autophagy induction can increase or decrease anticancer drug efficacy. Anticancer drug-induced autophagy is poorly characterized in osteosarcoma (OS). In this study, we investigated the impact of inhibition on camptothecin (CPT)-induced cytotoxicity OS. Autophagy-inhibited DLM8 and K7M3 metastatic murine OS cell lines were generated by infection with lentiviral shRNA directed against essential protein ATG5. Knockdown ATG5 expression was confirmed immunoblot LC3II proteins, respectively....
Chronic lymphocytic leukemia (CLL) cells are metabolically flexible and adapt to modern anticancer treatments. Bruton tyrosine kinase (BTK) B-cell lymphoma-2 (BCL-2) inhibitors have been widely used treat CLL, but CLL become resistant these treatments over time. CB-839 is a small-molecule glutaminase-1 (GLS-1) inhibitor that impairs glutamine use, disrupts downstream energy metabolism, impedes the elimination of reactive oxygen species.To investigate in vitro effects on cells, we tested...
Abstract Poly (ADP-ribose) polymerase inhibitors (PARPi) can encounter resistance through various mechanisms, limiting their effectiveness. Our recent research showed that PARPi alone induce drug by promoting autophagy. Moreover, our studies have revealed anaplastic lymphoma kinase (ALK) plays a role in regulating the survival of ovarian cancer cells undergoing Here, we explored whether ALK-inhibitor crizotinib could enhance efficacy targeting drug-induced autophagic cell and xenograft...
Autophagy is a catabolic process involved in cellular homeostasis. increased above homeostatic levels by chemotherapy, and this can either promote or inhibit tumor growth. We previously demonstrated that aerosol gemcitabine (GCB) has therapeutic effect against osteosarcoma (OS) lung metastases. However, some cells failed to respond the treatment persisted as isolated metastasis. Here, we examined mechanisms underlying dual role of chemotherapy-induced autophagy OS sought identify biomarkers...
The presence of the Philadelphia chromosome in patients with acute lymphoblastic leukemia (Ph+ALL) is a negative prognostic indicator. Tyrosine kinase inhibitors (TKI) that target BCR/ABL, such as imatinib, have improved treatment Ph+ALL and are generally incorporated into induction regimens. This approach has clinical responses, but molecular remissions seen less than 50% leaving few options event relapse. Thus, identification additional targets for therapeutic intervention potential to...
Background Poor outcomes for patients with ovarian cancer relate to dormant, drug‐resistant cells that survive after primary surgery and chemotherapy. Ovarian (OvCa) persist in poorly vascularized scars on the peritoneal surface depend autophagy nutrient deprivation. The authors have sought drugs target autophagic selectively eliminate residual disease. Methods By using unbiased small‐interfering RNA (siRNA) screens, observed knockdown of anaplastic lymphoma kinase (ALK) reduced survival...
Chemotherapy-induced autophagy is a proposed mechanism of chemoresistance and potential therapeutic target in osteosarcoma. We evaluated heat shock protein 27 (HSP27) autophagy-related proteins as predictors pathologic treatment response prognostic markers among osteosarcoma patients who received standard chemotherapy. analyzed 394 tumor specimens (pre-treatment, post-treatment, metastases) from 260 by immunohistochemistry for cytoplasmic light chain 3B (LC3B)-positive puncta, sequestosome 1...
Fas-associated protein with death domain (FADD) was first identified for its role in linking receptors to the apoptotic signaling pathway subsequent cell death.Later studies reported non-apoptotic functions FADD normal cells and cancer cells.Non-apoptotic osteosarcoma (OS) have not been reported.In this study, expression knocked down human CCHOSD, LM7, SaOS2 OS lines followed by assessment of sensitivity TNFα-or TRAIL-induced death.Knock significantly increased TNFα-induced LM7 lines.The...
<div>Abstract<p>Poly (ADP-ribose) polymerase inhibitors (PARPi) can encounter resistance through various mechanisms, limiting their effectiveness. Our recent research showed that PARPi alone induce drug by promoting autophagy. Moreover, our studies have revealed anaplastic lymphoma kinase (ALK) plays a role in regulating the survival of ovarian cancer cells undergoing Here, we explored whether ALK-inhibitor crizotinib could enhance efficacy targeting drug-induced autophagic cell...
<div>Abstract<p>Poly (ADP-ribose) polymerase inhibitors (PARPi) can encounter resistance through various mechanisms, limiting their effectiveness. Our recent research showed that PARPi alone induce drug by promoting autophagy. Moreover, our studies have revealed anaplastic lymphoma kinase (ALK) plays a role in regulating the survival of ovarian cancer cells undergoing Here, we explored whether ALK-inhibitor crizotinib could enhance efficacy targeting drug-induced autophagic cell...
<p>Supplementary Figure S3 shows the viability of ovarian cancer cells treated with other PARPi in combination Olaparib</p>
<p>Supplementary Figure S2 shows dose response curves, colony formation assays and viability of Olaparib resistant cells treated with crizotinib</p>
<p>Supplementary Figure S7 shows the effect of knocking down ALK on sensitivity ovarian cancer cells to Olaparib/crizotinib combination</p>
<p>Supplementary Figure S5 shows induction of ROS, DNA damage and apoptosis after treatment with Olaparib crizotinib</p>
<p>Supplementary Figure S5 shows induction of ROS, DNA damage and apoptosis after treatment with Olaparib crizotinib</p>
<p>Supplementary Figure S4 shows induction of autophagy after treatment with the combination Olaparib and crizotinib</p>
<p>Supplementary Figure S3 shows the viability of ovarian cancer cells treated with other PARPi in combination Olaparib</p>
<p>Supplementary Figure S6 shows the effect of combination Olaparib and crizotinib in tumor growth</p>
<p>Supplementary Figure S7 shows the effect of knocking down ALK on sensitivity ovarian cancer cells to Olaparib/crizotinib combination</p>
<p>Supplementary Figure S4 shows induction of autophagy after treatment with the combination Olaparib and crizotinib</p>
<p>Supplementary Figure S6 shows the effect of combination Olaparib and crizotinib in tumor growth</p>
<p>Supplementary Figure S1 shows CI values and IC50 of Olaparib Olaparib/crizotinib</p>