human
The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
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    INPUT: This study aimed to observe the effects of octreotide ( OCT ) on cisplatin resistance reversal of cancer cells in vitro and in nude mice in vivo . MTT method and flow cytometry were used to investigate the effect of cisplatin , OCT or the combination of these two compounds on the proliferation and apoptosis of SKOV3-DDP cells . The size and weight of xenograft tumors from the nude mice model were measured . Real-time PCR was used to detect the mRNA expression of SSTR2 , MDR1 , MRP2 , GST-pi and EGFR in SKOV3/DDP cells following the different treatment . At the concentration of 2.5-20 g/ml , OCT significantly reduced IC50 ( p &lt ; 0.05 ) and promoted apoptosis ( p &lt ; 0.05 ) of SKOV3-DDP cells ' response to cisplatin . Unchanged expression was found in SSTR2 on the SKOV3/DDP cell in vitro after OCT treatment , but increased expression in vivo ( p &lt ; 0.05 ) . OCT increased GST-pi expression ( p &lt ; 0.05 ) and reduced MRP2 and EGFR expression ( p &lt ; 0.05 ) in a dose-dependent manner . The similar results were obtained in mice in vivo experiment , except the reduced expression of GST-pi . It is suggested that OCT could inhibit ovarian cancer proliferation and promote apoptosis , via the cell surface SSTR2 , and reverse cisplatin resistance through inhibition of MRP2 , EGFR , and even GST-pi expressions .
    OUTPUT:

agent
resisting cell death;sustaining proliferative signaling
The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
    ###
    INPUT: This study aimed to observe the effects of octreotide ( OCT ) on cisplatin resistance reversal of cancer cells in vitro and in nude mice in vivo . MTT method and flow cytometry were used to investigate the effect of cisplatin , OCT or the combination of these two compounds on the proliferation and apoptosis of SKOV3-DDP cells . The size and weight of xenograft tumors from the nude mice model were measured . Real-time PCR was used to detect the mRNA expression of SSTR2 , MDR1 , MRP2 , GST-pi and EGFR in SKOV3/DDP cells following the different treatment . At the concentration of 2.5-20 g/ml , OCT significantly reduced IC50 ( p &lt ; 0.05 ) and promoted apoptosis ( p &lt ; 0.05 ) of SKOV3-DDP cells ' response to cisplatin . Unchanged expression was found in SSTR2 on the SKOV3/DDP cell in vitro after OCT treatment , but increased expression in vivo ( p &lt ; 0.05 ) . OCT increased GST-pi expression ( p &lt ; 0.05 ) and reduced MRP2 and EGFR expression ( p &lt ; 0.05 ) in a dose-dependent manner . The similar results were obtained in mice in vivo experiment , except the reduced expression of GST-pi . It is suggested that OCT could inhibit ovarian cancer proliferation and promote apoptosis , via the cell surface SSTR2 , and reverse cisplatin resistance through inhibition of MRP2 , EGFR , and even GST-pi expressions .
    OUTPUT:
