Pub. Date : 2020 Apr 5
PMID : 32017938
8 Functional Relationships(s)Download |
Sentence | Compound Name | Protein Name | Organism |
| 1 | Long non-coding RNA ROR confers arsenic trioxide resistance to HepG2 cells by inhibiting p53 expression. | Arsenic Trioxide | tumor protein p53 | Homo sapiens |
| 2 | In this study, We found that cellular apoptosis was increased by arsenic trioxide in liver cancer HepG2 cells; P53 expression was also increased by arsenic trioxide at both mRNA level and protein level, indicating that P53-dependent apoptosis is the main mechanism for arsenic trioxide to induce cytotoxicity in liver cancer HepG2 cells. | Arsenic Trioxide | tumor protein p53 | Homo sapiens |
| 3 | In this study, We found that cellular apoptosis was increased by arsenic trioxide in liver cancer HepG2 cells; P53 expression was also increased by arsenic trioxide at both mRNA level and protein level, indicating that P53-dependent apoptosis is the main mechanism for arsenic trioxide to induce cytotoxicity in liver cancer HepG2 cells. | Arsenic Trioxide | tumor protein p53 | Homo sapiens |
| 4 | In this study, We found that cellular apoptosis was increased by arsenic trioxide in liver cancer HepG2 cells; P53 expression was also increased by arsenic trioxide at both mRNA level and protein level, indicating that P53-dependent apoptosis is the main mechanism for arsenic trioxide to induce cytotoxicity in liver cancer HepG2 cells. | Arsenic Trioxide | tumor protein p53 | Homo sapiens |
| 5 | In this study, We found that cellular apoptosis was increased by arsenic trioxide in liver cancer HepG2 cells; P53 expression was also increased by arsenic trioxide at both mRNA level and protein level, indicating that P53-dependent apoptosis is the main mechanism for arsenic trioxide to induce cytotoxicity in liver cancer HepG2 cells. | Arsenic Trioxide | tumor protein p53 | Homo sapiens |
| 6 | In this study, We found that cellular apoptosis was increased by arsenic trioxide in liver cancer HepG2 cells; P53 expression was also increased by arsenic trioxide at both mRNA level and protein level, indicating that P53-dependent apoptosis is the main mechanism for arsenic trioxide to induce cytotoxicity in liver cancer HepG2 cells. | Arsenic Trioxide | tumor protein p53 | Homo sapiens |
| 7 | Through the knock-down of long non-coding RNA ROR by siRNA, we revealed that the activated long non-coding RNA ROR ameliorated arsenic trioxide-induced apoptosis by inhibiting P53 expression. | Arsenic Trioxide | tumor protein p53 | Homo sapiens |
| 8 | Together, our study reported that long non-coding RNA ROR conferred arsenic trioxide resistance to liver cancer cells through inhibiting P53 expression, and long non-coding RNA ROR might be a novel sensitizing target for liver cancer treatment. | Arsenic Trioxide | tumor protein p53 | Homo sapiens |