GSTP1 overexpression

Intriguingly, Auranofin increased the expression of glutathione S-transferase pi-1 (GSTP-1), a target of PPL. Combining Auranofin with PPL synergistically decreased IC50s to a nanomolar range in GSCs, supporting the potential to repurpose Auranofin and PPL in GBM.

To highlight possible correlations of type 2 diabetes mellitus (T2DM) with microscopic / macroscopic characteristics of colorectal cancer tissues, along with the expression of Ten-Eleven Translocation 2 (TET2) and glutathione-S-transferase pi (GST-pi) proteins.

These changes increase the resistance of pancreatic cancer cells and xenograft tumors to IR. Our findings indicate that ferroptosis participates in irradiation-induced cell death and that GSTP1 prevents IR-induced death of pancreatic cancer cells by inhibiting ferroptosis.

Gene enrichment and network analysis associated ABCB1 with ABC transporters and LncRNA-mediated therapeutic resistance (WP3672), while CYP1B1 was linked to ovarian steroidogenesis, tryptophan metabolism, steroid hormone biosynthesis, benzo(a)pyrene metabolism, the sulindac metabolic pathway, and the estrogen receptor pathway, which are associated with drug resistance. These findings underscore the susceptibility of cancer patients to drug resistance due to increased ABCB1 and CYP1B1 expression in tumor samples from patients in the poor-responders category that affects associated molecular pathways. The potent molecular interactions of ABCB1 and CYP1B1 with docetaxel further emphasize the potential basis for chemotherapy resistance.

NBDHEX exhibits anti-cancer activity by selectively inhibiting glutathione-S-transferase pi (GSTP1), which is overexpressed in cancer cells and responsible for the inactivation of chemotherapeutic drugs. The sustained release of NBDHEX from the prodrug would be useful for ameliorating the off-target side-effects of NBDHEX.

In conclusion, our study provides a robust and reliable methylation-based diagnostic model for PCa. This model holds promise as an improved approach for screening and diagnosing PCa, potentially enhancing early detection and patient outcomes, as well as for an advanced clinical management for PCa in the framework of predictive, preventive and personalised medicine.

The results demonstrated that the incorporation of TMP into EXOs exhibited an anti‑ovarian cancer effect and markedly enhanced the antitumor efficacy of paclitaxel (PTX)...Overall, EXO‑TMP exhibited direct targeting capabilities towards A2780T cells and effectively reduced their drug resistance. EXOs‑TMP provide a novel and effective drug delivery pathway for reversing drug resistance in ovarian cancer.

This study discusses novel mechanism of action by which PL acts on CSCSs. Taken together our study provides insight into development of PL based nanomedicine which could be exploited in clinics to achieve complete eradication of TNBC by targeting CSCs.

In addition, targeting GSTP1 with the inhibitor NBDHEX effectively rescued the cisplatin resistance induced by VPS13C deficiency. Overall, our findings provide insights into the underlying mechanisms of VPS13C in cisplatin resistance and identify VPS13C as a promising candidate for the treatment of chemoresistance in cervical cancer.

These results demonstrate that methylation density in the GSTP1 CpG island in PIN was intermediate relative to that in normal prostate epithelium/PIA and CaP lesions. These results are consistent with gradual spreading of DNA methylation centered at the SP1/AP1 transcription factor binding sites in precursor lesions, with subsequent spreading of methylation across the entire CpG island in transition to CaP.

Using patient-derived organoids from an ALK-translocated LUAD, the therapeutic potential of a specific GSTP1 inhibitor ezatiostat in combination treatment with the ALK inhibitor crizotinib is demonstrated. This study demonstrates GSTP1 to be a promising therapeutic target for long-term control of LUAD through targeting CSCs.

Overall, our study is the first to reveal that catalpol can promote OL generation and myelination and contributes to the crucial regulatory process of GEF-Cdc42/Rac1 signaling expression and activation. Therefore, catalpol is a promising drug candidate for the potential treatment of demyelinating diseases.

The present study demonstrated that HDEA could protect mouse skin fibroblasts (L929) and human immortalized keratinocytes (HaCaT) against photoaging due to ultraviolet A and B (UVA and UVB) by reducing intracellular reactive oxygen species (ROS) and expressions of matrix metalloproteinases (MMP1 and MMP3), as well as increasing Nrf2 nuclear translocation, upregulations of mRNA transcripts of antioxidant enzymes, including superoxide dismutase (SOD), heme oxygenase (HMOX) and glutathione S-transferase pi1 (GSTP1), and procollagen synthesis. The results indicate that HDEA has the potential to protect skin cells from UV irradiation through the activation of the Nrf2 pathway, which leads to decreasing intracellular ROS and MMP production, along with the restoration of skin collagen.

Pathway analysis elucidated that ajoene targets functional and signaling pathways that are implicated in cancer cell survival, specifically cellular processes, metabolism, and genetic information processing pathways. The results of this study provide mechanistic insights into the character of the anti-cancer activity of the natural dietary compound ajoene.

Furthermore, we found that 1, 2 and 3 could suppress cell proliferation and also induce mitochondrial dysfunction as well as oxidative stress, eventually leading to cellular apoptosis. Taken together, this study revealed that sesquiterpene lactones from E. scaber could be a promising therapeutic strategy for the treatment of glioma by targeting GSTP1.

NBDHEX serves as a good candidate for combination with adriamycin, offering new insights for breast cancer treatment.

Such proteins included complement C1q sub-components and GSTP1. This study provides a platform for further work, utilising larger sample sets across different treatment regimens for oesophageal cancer, that will aid the development of 'treatment response prediction assays' for stratification of OAC patients prior to chemotherapy.

Enrolment commenced November 2021. The results of this trial will generate data on the clinical utility of mGSTP1 as a novel biomarker to guide treatment de-escalation in metastatic CRPC.

Our results showed that overexpression of GSTpi in cells by transfecting DNA vector decreased the DNA damage level after methyl methanesulfonate (MMS) or adriamycin (ADR) treatment...Finally, GSTpi blocked the cell cycle in the G2/M phase to allow more time for DNA damage repair. Thus, our finding revealed the novel mechanism of GSTpi via its Ser184 phosphorylation to protect cells from cell death during DNA damage and it enriches the function of GSTpi in drug resistance.

Here, we have studied, for the first time, the proteome reactivity of cyclopropenones in live cells and discovered that the cyclopropenone warhead can specifically and efficiently modify a triple-negative breast cancer driver, glutathione S-transferase pi-1 (GSTP1), by covalently binding at the catalytic active site. Further structure optimization and signaling pathway validation have led to the discovery of potent inhibitors of GSTP1.

2D Ti C can reverse NSCLC chemoresistance both in vitro and in vivo, suggesting that it may potentially become a novel and effective means to treat chemoresistant NSCLC in the clinic.

The competitive endogenous RNA (ceRNA) mechanism indicated that circ-CHI3L1.2 targets the micro-RNA (miR)-340-5p-lysophosphatidic acid acyltransferase β (LPAATβ) axis, and inhibition of miR-340-5p alleviates the effect of circ-CHI3L1.2 knockdown. In conclusion, circ-CHI3L1.2 levels were increased in cisplatin-resistant osteosarcoma cells and circ-CHI3L1.2 knockdown sensitized cisplatin-resistant osteosarcoma cells to cisplatin through the miR-340-5p-LPAATβ axis.

We analyzed cells at 72h of co-culture, MM cells (OPM-2, U266, AMO-1) with MSCs or treatments with cytostatics, bortezomib (BTZ), melphalan and lenalidomide. Further investigations will reveal behavior of MMs adhered to MSCs. Increased β-galactosidase activity and variable alkaline phosphatase activity in MSCs after co-culture suggests MM-MSC interactions may contribute to the senescent profile of MSC Conclusion Although MSCs and cytostatics might show similar effects in terms of contribution to the chemoresistance-related molecules, our results imply MSCs bring additional complexity to MM populations with distinct stem cell-related properties.

We analyzed cells at 72h of co-culture, MM cells (OPM-2, U266, AMO-1) with MSCs or treatments with cytostatics, bortezomib (BTZ), melphalan and lenalidomide. Further investigations will reveal behavior of MMs adhered to MSCs. Increased β-galactosidase activity and variable alkaline phosphatase activity in MSCs after co-culture suggests MM-MSC interactions may contribute to the senescent profile of MSC Conclusion Although MSCs and cytostatics might show similar effects in terms of contribution to the chemoresistance-related molecules, our results imply MSCs bring additional complexity to MM populations with distinct stem cell-related properties.

We analyzed cells at 72h of co-culture, MM cells (OPM-2, U266, AMO-1) with MSCs or treatments with cytostatics, bortezomib (BTZ), melphalan and lenalidomide. Further investigations will reveal behavior of MMs adhered to MSCs. Increased β-galactosidase activity and variable alkaline phosphatase activity in MSCs after co-culture suggests MM-MSC interactions may contribute to the senescent profile of MSC Conclusion Although MSCs and cytostatics might show similar effects in terms of contribution to the chemoresistance-related molecules, our results imply MSCs bring additional complexity to MM populations with distinct stem cell-related properties.

We analyzed cells at 72h of co-culture, MM cells (OPM-2, U266, AMO-1) with MSCs or treatments with cytostatics, bortezomib (BTZ), melphalan and lenalidomide. Further investigations will reveal behavior of MMs adhered to MSCs. Increased β-galactosidase activity and variable alkaline phosphatase activity in MSCs after co-culture suggests MM-MSC interactions may contribute to the senescent profile of MSC Conclusion Although MSCs and cytostatics might show similar effects in terms of contribution to the chemoresistance-related molecules, our results imply MSCs bring additional complexity to MM populations with distinct stem cell-related properties.

PCSK9 inhibited HCC cell proliferation, cell cycle progression, and apoptosis by interacting with GSTP1 and suppressing JNK signaling, suggesting that PCSK9 might act as a tumor suppressor and be a therapeutic target in HCC patients.

In conclusion, 2AAF induces the early appearance of HPC markers and as a result, accelerates the hepatocarcinogenesis induced by DEN in the rat. Thus, since 2AAF simultaneously administrated with DEN enriches HPC during hepatocarcinogenesis, we propose that DEN + 2AAF protocol might be a useful tool to investigate the cellular origin of HCC with progenitor features.

Preliminary findings for three SNPs rs2231142 (in ABCG2, ATP binding cassette subfamily G member 2), rs1800440 (in CYP1B1, Cytochrome P450 family 1 subfamily B member 1) and rs1695 (in GSTP1, Glutathione S-transferase pi 1) demonstrated genetic differences across the lines, based on either ethnicity of derivation (four African American-derived versus four Caucasian-derived), hormone receptor positivity (ER+/PR+/HER2+ versus ER+/PR+/HER2- versus ER-/PR-/HER2+) or triple-negative subtype (ER-/PR-/HER2-) classification. We are currently determining the targetable interactions between these SNPs and others with allelic differences, and metabolic responses to paclitaxel, which will enable us to test strategies for by-passing these impairments to improve treatment efficacy.

, 95% CI = 0.36, 0.17-0.78, P for trend = 0.013; lipophilic ORAC = 0.58, 0.37-0.93, P for trend = 0.021; total phenolics = 0.38, 0.17-0.83, P for trend = 0.019). Our findings indicate that dietary ORAC intake may be inversely associated with the risk of gastric cancer altered by genetic variants of GSTP1, providing new intervention strategies for gastric cancer patients.

TGF‑β‑induced oxidative stress was suppressed by increasing glutathione S‑transferase Pi 1 and reducing peroxiredoxin 1. Collectively, the present results indicated that AAV‑shRNAs were effective in modulating liver fibrosis by reducing oxidative stress, inflammation and activating the PPAR signaling pathway.

In silico analysis confirmed commonly deregulated proteins in the ventral prostate of old rats and patients with prostate cancer. In conclusion, the increase in oxidative stress associated with an imbalance of sex hormones may contribute to prostate carcinogenesis in offspring, highlighting early-life malnutrition as a key risk factor for this malignance.

The results demonstrated that GSTP1 polymorphisms were useful predictors of severe events. Screening of single-nucleotide polymorphisms of GSTP1 in colorectal cancer patients before chemotherapy may help to realize personalized therapy.

These outcomes demonstrate an eleven-gene molecular panel that predicts the patients' prospective survival following pancreatic resection for PDAC.

Moreover, GSTP1 overexpression was observed to reverse the effects of LINC01270 overexpression on EC cells and their response to 5-FU. Taken together, this study shows that inhibition of LINC01270 can lead to suppression of EC progression via demethylation of GSTP1, highlighting this lncRNA as a potential target for EC treatment.

Thus, MNPC, a dual inhibitor for both NQO1 and GSTP1, provides a novel lead compound for treating GBM via the exploitation of specific vulnerabilities created by mutant EGFR.

Mutant GSTP1 genotype was an independent prognostic factor for increased HCC risk which can be used in a risk assessment model for HCC. Plasma GSH presents insufficient sensitivity and specificity for HCC.