PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32646966-6 2020 Cell lines with low SHP2 expression and higher levels of pYAPY357 were resistant to gemcitabine and cisplatin. Cisplatin 100-109 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 20-24 32646966-7 2020 In CCA cells with high levels of SHP2, pharmacologic inhibition or genetic deletion of SHP2 increased YAPY357 phosphorylation and expression of YAP target genes, including the anti-apoptotic regulator MCL1, imparting resistance to gemcitabine and cisplatin. Cisplatin 247-256 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 87-91 25561980-10 2015 Knockdown of Shp-2 in HepG2 cells resulted in upregulation of mitochondrial TERT expression and increased resistance to cisplatin (CDDP) and 5-fluorouracil (5-FU) (resistance indices, 2.094 and 1.863, respectively). Cisplatin 120-129 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 13-18 28085101-12 2017 Furthermore, knockdown of Shp2 attenuated cisplatin-sensitivity of ESCC cells. Cisplatin 42-51 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 26-30 31564571-0 2019 Shp2 expression is upregulated in cervical cancer, and Shp2 contributes to cell growth and migration and reduces sensitivity to cisplatin in cervical cancer cells. Cisplatin 128-137 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 0-4 31564571-0 2019 Shp2 expression is upregulated in cervical cancer, and Shp2 contributes to cell growth and migration and reduces sensitivity to cisplatin in cervical cancer cells. Cisplatin 128-137 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 55-59 31564571-5 2019 Shp2 knockdown inhibited cell growth and migration and enhanced sensitivity to cisplatin in the HeLa and SiHa cervical cancer cell lines. Cisplatin 79-88 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 0-4 31564571-8 2019 In conclusion, Shp2 is involved in the occurrence and development of cervical cancer and may confer cisplatin resistance in cervical cancer. Cisplatin 100-109 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 15-19 29207183-0 2018 Src homology phosphotyrosyl phosphatase 2 mediates cisplatin-related drug resistance by inhibiting apoptosis and activating the Ras/PI3K/Akt1/survivin pathway in lung cancer cells. Cisplatin 51-60 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 0-41 29207183-3 2018 To explore the role of Src homology phosphotyrosyl phosphatase 2 (SHP2) in the development of cisplatin resistance in lung cancer and the underlying mechanism, we established stable SHP2-overexpressing H446-SHP2-OE cells and SHP2-knockdown H446/CDDP-SHP2-shRNA cells derived from H446 and H446/CDDP (cisplatin-resistant) parental lung cancer cells. Cisplatin 94-103 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 66-70 29207183-6 2018 As a result, the 50% inhibitory concentration (IC50) of the H446-SHP2-OE cells exposed to CDDP increased from 1.01 to 1.218 microg/ml vs. the H446-control vector cells. Cisplatin 90-94 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 65-69 29207183-7 2018 The percentage of apoptotic cells was smaller in the H446-SHP2-OE cells vs. the H446-control vector cells after cisplatin challenge. Cisplatin 112-121 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 58-62 29207183-9 2018 Furthermore, the IC50 of the H446/CDDP-SHP2-shRNA cells exposed to CDDP decreased from 11.92 to 4.382 microg/ml vs. the H446/CDDP-mock cells. Cisplatin 67-71 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 34-43 29207183-10 2018 There were significantly more apoptotic cells among the H446/CDDP-SHP2-shRNA cells vs. the H446/CDDP-mock cells exposed to cisplatin. Cisplatin 123-132 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 61-70 29207183-12 2018 In addition, the expression of pAkt1 and survivin in the H446, H446/CDDP and H446/CDDP-mock cells was increased upon exposure to cisplatin however, a corresponding change was not observed in the H446/CDDP-SHP2-shRNA cells. Cisplatin 129-138 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 200-209 29207183-13 2018 Upon Ras RNA silencing with cisplatin, the Ras expression was significantly decreased in the H446, H446-SHP2-OE and H446/CDDP cells. Cisplatin 28-37 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 104-108 29207183-15 2018 In conclusion, SHP2 is a new cisplatin resistance-related phosphatase in lung cancer, which inhibits apoptosis by activating the Ras/PI3K/Akt1/survivin signaling pathway. Cisplatin 29-38 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 15-19 28423588-0 2017 Shp2 confers cisplatin resistance in small cell lung cancer via an AKT-mediated increase in CA916798. Cisplatin 13-22 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 0-4 28423588-3 2017 Here, we show that Shp2 plays an important role in inducing resistance to cisplatin-based chemotherapy via the SHP2-AKT-CA916798 pathway. Cisplatin 74-83 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 19-23 28423588-3 2017 Here, we show that Shp2 plays an important role in inducing resistance to cisplatin-based chemotherapy via the SHP2-AKT-CA916798 pathway. Cisplatin 74-83 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 111-115 28423588-4 2017 In an SCLC cell line, overexpression of Shp2 induced cisplatin resistance and the increased expression of AKT, pAKT, pmTOR, and CA916798. Cisplatin 53-62 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 40-44 28423588-5 2017 Conversely, depletion of Shp2 in a cisplatin-resistant cell line via RNA interference increased cisplatin sensitivity and decreased AKT, pAKT, pmTOR, and CA916798 expression levels. Cisplatin 35-44 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 25-29 28423588-5 2017 Conversely, depletion of Shp2 in a cisplatin-resistant cell line via RNA interference increased cisplatin sensitivity and decreased AKT, pAKT, pmTOR, and CA916798 expression levels. Cisplatin 96-105 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 25-29 28423588-10 2017 Together, our findings indicate that Shp2 induces cisplatin resistance in SCLC patients via the SHP2-AKT-CA916798 pathway. Cisplatin 50-59 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 37-41 28423588-10 2017 Together, our findings indicate that Shp2 induces cisplatin resistance in SCLC patients via the SHP2-AKT-CA916798 pathway. Cisplatin 50-59 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 96-100 25561980-10 2015 Knockdown of Shp-2 in HepG2 cells resulted in upregulation of mitochondrial TERT expression and increased resistance to cisplatin (CDDP) and 5-fluorouracil (5-FU) (resistance indices, 2.094 and 1.863, respectively). Cisplatin 131-135 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 13-18 19909727-0 2010 Selective activation of SHP2 activity by cisplatin revealed by a novel chemical probe-based assay. Cisplatin 41-50 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 24-28 23189174-4 2012 More detailed studies revealed that SHP2 was also important for the maintenance of the checkpoint after DNA damage induced by cisplatin or ionizing radiation in HeLa cells. Cisplatin 126-135 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 36-40 19909727-8 2010 Although the role of SHP2 activation by cisplatin treatments is still unclear to us, our results provide the first direct evidence for the activation of SHP2 during cisplatin treatments. Cisplatin 40-49 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 21-25 19909727-8 2010 Although the role of SHP2 activation by cisplatin treatments is still unclear to us, our results provide the first direct evidence for the activation of SHP2 during cisplatin treatments. Cisplatin 165-174 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 153-157 19909727-4 2010 Here, by combining LCL2 with a SHP2 specific antibody, we established an assay system that enables the direct monitoring of SHP2 activity upon cisplatin treatment of cancer cells. Cisplatin 143-152 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 31-35 19909727-4 2010 Here, by combining LCL2 with a SHP2 specific antibody, we established an assay system that enables the direct monitoring of SHP2 activity upon cisplatin treatment of cancer cells. Cisplatin 143-152 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 124-128 19909727-6 2010 Using this assay, we found SHP2 activity was selectively activated by cisplatin. Cisplatin 70-79 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 27-31 19909727-7 2010 Moreover, the activation of SHP2 appeared to be specific for cisplatin as other DNA damage agents failed to activate the activity. Cisplatin 61-70 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 28-32 16260787-4 2005 Mutant embryonic fibroblasts with the Exon 3 deletion mutation in SHP-2 showed decreased apoptosis and diminished G2/M arrest in response to cisplatin treatment. Cisplatin 141-150 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 66-71 16260787-7 2005 Furthermore, inhibition of the catalytic activity of endogenous SHP-2 in WT cells by overexpression of SHP-2 C459S greatly decreased cell death but not G2/M arrest induced by cisplatin. Cisplatin 175-184 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 64-69 16260787-11 2005 Embryonic stem cells with the SHP-2 deletion mutation showed markedly decreased sensitivity to cisplatin-induced apoptosis, attributed to impaired induction of p73 but not p53. Cisplatin 95-104 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 30-35 12594211-4 2003 Following cisplatin treatment, induction of p73 and its downstream effector p21(Cip1) was essentially blocked in SHP-2 mutant cells. Cisplatin 10-19 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 113-118