Objective To clarify the effect of miR-181b on the biological function of SCLC, to detect and verify its downstream target gene ACE2, and to explore the effect of clinical resistance on SCLC in order to find new specific diagnostic markers and therapeutic targets.
Methods 1. Collect blood samples from 30 SCLC patients and 30 normal persons in our department from 2017 to 2019 to detect the expression level of miR-181b; 2. Detect the expression level of miR-181b in SCLC cells by RT-PCR, and Screening of downstream target genes used by gene chip, verification with luciferase and Western Blot; 3. Collect the general data of 30 SCLC patients and 30 healthy people (control group),the patients were diagnosed by pathology and undergoing EC protocol in the Department of Thoracic Surgery and Oncology of our hospital to detect the expression level of mir-181b in different periods; 4. In the SCLC cell line and the SCLC mouse model constructed, different concentrations of EC chemotherapy and ACEI drugs were administered to detect the sensitivity of drug resistance and non-drug resistance.
Results 1. The expression level of miR-181b in SCLC patients was lower than normal people; 2. The expression level of miR-181b in SCLC cell lines was lower than normal cells; ACE2 was verified as a downstream target of miR-181b by gene chip screening; 3. miR-181b is low-expressed in SCLC patients, first-line chemotherapy can promote its recovery, but cannot repair to normal levels, and miR-181b has a certain effect on SCLC chemotherapy sensitivity; 4. miR-181b can enhance the drug sensitivity of SCLC drug-resistant cells, the application of ACEI should increase the risk of SCLC drug-resistant.
Conclusion 1. miR-181b has a low expression level in SCLC, and it can directly target the gene ACE2 to affect the biological characteristics of SCLC; 2. miR-181b is lowly expressed in SCLC patients, and first-line chemotherapy can promote it recovery, but cannot repair to normal levels, and ACEI drugs can increase the risk of SCLC drug-resistant.

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Posted 27 Jul, 2020
Posted 27 Jul, 2020
Objective To clarify the effect of miR-181b on the biological function of SCLC, to detect and verify its downstream target gene ACE2, and to explore the effect of clinical resistance on SCLC in order to find new specific diagnostic markers and therapeutic targets.
Methods 1. Collect blood samples from 30 SCLC patients and 30 normal persons in our department from 2017 to 2019 to detect the expression level of miR-181b; 2. Detect the expression level of miR-181b in SCLC cells by RT-PCR, and Screening of downstream target genes used by gene chip, verification with luciferase and Western Blot; 3. Collect the general data of 30 SCLC patients and 30 healthy people (control group),the patients were diagnosed by pathology and undergoing EC protocol in the Department of Thoracic Surgery and Oncology of our hospital to detect the expression level of mir-181b in different periods; 4. In the SCLC cell line and the SCLC mouse model constructed, different concentrations of EC chemotherapy and ACEI drugs were administered to detect the sensitivity of drug resistance and non-drug resistance.
Results 1. The expression level of miR-181b in SCLC patients was lower than normal people; 2. The expression level of miR-181b in SCLC cell lines was lower than normal cells; ACE2 was verified as a downstream target of miR-181b by gene chip screening; 3. miR-181b is low-expressed in SCLC patients, first-line chemotherapy can promote its recovery, but cannot repair to normal levels, and miR-181b has a certain effect on SCLC chemotherapy sensitivity; 4. miR-181b can enhance the drug sensitivity of SCLC drug-resistant cells, the application of ACEI should increase the risk of SCLC drug-resistant.
Conclusion 1. miR-181b has a low expression level in SCLC, and it can directly target the gene ACE2 to affect the biological characteristics of SCLC; 2. miR-181b is lowly expressed in SCLC patients, and first-line chemotherapy can promote it recovery, but cannot repair to normal levels, and ACEI drugs can increase the risk of SCLC drug-resistant.

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