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P5091 activates apoptotic process. 37 / 37
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"P5091 treatment effectively induces apoptosis in both TP53 mutated MEC-1 and TP53-wild-type EHEB cell lines and, remarkably, is highly effective in del17p CLL primary CD19 + lymphocytes, with an apoptotic induction ' potency ' like the one observed in TP53-wild type CLL samples."
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"Notable examples include FOXO-DRI, which activates FOXO transcription factors involved in regulating the cell cycle and apoptosis [219]; UBX0101, known for its ability to selectively induce apoptosis in senescent cells, offering therapeutic promise for age-related diseasesm [219]; and P22077/P5091, which inhibit MDM2 to enhance P53 activity and promote the removal of senescent cells [220]."
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"P5091 is an inhibitor of USP7 and USP47 ( Chauhan et al., 2012; Weinstock et al., 2012 ) and was found to induce apoptosis of multiple myeloma cells resistant to the 20S proteasome inhibitor bortezomi[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Meanwhile, P5091 induced apoptosis in multiple myeloma cells resistant to conventional and Bortezomib therapies."
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"The Z-VAD-FMK pan-caspase inhibitor interfered with the P5091 induced citotoxicity in SCLC cells; moreover, the caspase 3 is activated upon P5091 treatment of SCLC cells, overall suggesting that the a[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"The detection at western blot of the cleaved fragments of cytochrome C and caspase 8 suggests that the P5091 triggered apoptosis was mediated either in mitochondria dependent and mitochondria independ[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Taken together, all data demonstrated that the low dose P5091 induced apoptosis via the activation of the p53 pathway in senescent HDF cells.The progression of wound closure following the topical appl[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"P5091 induced apoptosis in BTZ resistant MM cells, supporting the concept that alternate (upstream) targeting of the UPS has potential utility in cancer therapy."
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"Moreover, the deubiquitinase USP7 has been shown to deubiquitinate several key cancer proteins, and P5091, a highly specific inhibitor of USP7, induced apoptosis in multiple myeloma cells."
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"26 The E3 inhibitor lenalidomide , which targets MARCH 1 , has been used to treat hematologic malignancies ; 88 the DUB inhibitor curcumin destabilizes CSN5 and improves the efficacy of immunotherapy in breast cancer , melanoma , and colon cancer ; 53 P5091 , which targets USP7 , induces apoptosis in multiple myeloma cell lines.134 Given the success of these E3 inhibitors and DUB inhibitors , increasing efforts have been made to design and develop novel small molecule inhibitors that are expected to modulate immune checkpoint pathways ."
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"Besides, P5091, a selective USP7 inhibitor, was found to induce apoptosis and overcome bortezomib resistance in MM cells."
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"Meanwhile , P5091 induced apoptosis in multiple myeloma cells resistant to conventional and Bortezomib therapies ."
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"Overall, these cell experimental data explained the biological mechanism by which P5091 selectively induced senescence HDF cell apoptosis by activating the p53 signaling pathway, which has clinical va[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"P5091 induces apoptosis of multiple myeloma cells that are resistant to bortezomib, a 20S proteasome inhibitor."
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"In vitro, P5091 inhibits proliferation of CRC cells and induces apoptosis."
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"It is very probable that , P5091 effects are p53-independent , as P5091 promoted apoptosis in TP53-mutated MEC-1 cells ."
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"It is very probable that, P5091 effects are p53 independent, as P5091 promoted apoptosis in TP53 mutated MEC-1 cells."
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"Importantly , P5091 induces apoptotic cell death in patient multiple myeloma cells resistance to bortezomib , lenalidomide , and dexamethasone [ 213 ] ."
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"P5091 effectively suppressed the growth of ovarian cancer cells, caused cell cycle blockage, and induced necrosis and apoptosis with more severe phenotypes observed in HeyA8 cells with wild-type p53 than in OVCAR-8 cells with mutant p53."
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"P5091 induces cell apoptosis in multiple myeloma cells and overcomes bortezomib resistance by inhibiting Usp7 activity [19] ."
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"Our observation that P5091 markedly promoted apoptosis in TP53 mutated MEC-1 cells suggests that P5091 effects are p53 independent in CLL."
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"The IC50 of SHG-140 and T98G cells were 1.2 µM and 1.59 µM, respectively, when treated with P5091 for 48 h. Based on IC50, SHG-140 and T98G cells were treated with P5091 for 48 h at 1, 2, and 4 µM. To explore whether P5091 induced apoptosis in GBM cells, we used Annexin V-FITC/PI flow cytometry."
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"After establishing that P5091 triggers apoptosis in lymphoma and leukemia cells, we examined if the induced apoptosis resulted from DNA damage."
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"All of these results proved that both P5091 and anti-PD-1 treatment enhanced tumor proliferation inhibition and apoptosis in vivo."
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"32 Our study here aimed to examine the effect of P5091 on antitumor immunity and its possible role in cancer immunotherapy.In our study, we found that P5091 promoted colon cancer cell apoptosis and death in CT26 xenografted mice and that the effect was similar when compared to an anti-PD-1-treated group."
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"In studies of multiple myeloma, P5091 was demonstrated to induce apoptosis in both bortezomib refractory multiple myeloma cells and animal tumor models."
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"P5091 was found to induce apoptosis in various MM cell lines as well as ex vivo cells, including those resistant to previous treatments [XREF_BIBR]."
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"For example, P5091 was able to induce apoptosis in non-neuroendocrine lung (L-NEC) tumor while P22077 reactivated p53 and induced apoptosis in human neuroblastoma (NB) and overcame cellular chemoresis[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Furthermore, P5091 induced apoptosis in various multiple myeloma (MM) cell lines as well as patient MM cells, including those resistant to prior treatments such as bortezomib, lenalidomide, and dexamethasone 89."
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"Since our in vitro data showed that P5091 triggers apoptosis in p53-null ARP-1 MM cells, we evaluated whether P5091 similarly affects the growth of ARP-1 cells in vivo."
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"P5091 triggers apoptosis in MM cells even in the presence of the MM-host BM microenvironment."
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"Importantly, P5091 inhibits USP7 activity in vivo and induces apoptosis in MM xenografted tumors."
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"This is consistent with the previous study [28] , namely that P5091-induced apoptosis is independent of p53 status."
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"Also in primary cells, P5091 treatment strongly promoted apoptosis while B-lymphocytes from normal individuals were unaffected."
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"P5091 also induces apoptosis in multiple myeloma cells that are previously impervious to traditional therapies and bortezomib treatment."
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"P5091 suppressed in vivo tumor growth [XREF_BIBR], caused apoptosis of Multiple Myeloma (MM) cells, and prolonged survival in xenograft models [XREF_BIBR]."
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"P5091 treatment significantly increased apoptosis induced by cisplatin or doxorubicin (Fig. 5E; Fig. S5I)."
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