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Application of ATF3 as target site in preparing taxol chemosensitization medicine for treating nasopharynx cancer

A target site, paclitaxel technology, applied in the field of biomedicine, can solve the problems of paclitaxel chemosensitivity research is rare, the specific mechanism is not clear, etc.

Pending Publication Date: 2018-09-04
THE THIRD XIANGYA HOSPITAL OF CENT SOUTH UNIV
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

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Problems solved by technology

Although some studies have found that lncRNA can participate in the regulation of multidrug resistance, the research on lncRNA regulation of paclitaxel chemotherapy sensitivity in nasopharyngeal carcinoma is very rare and the specific mechanism is still unclear.

Method used

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  • Application of ATF3 as target site in preparing taxol chemosensitization medicine for treating nasopharynx cancer
  • Application of ATF3 as target site in preparing taxol chemosensitization medicine for treating nasopharynx cancer
  • Application of ATF3 as target site in preparing taxol chemosensitization medicine for treating nasopharynx cancer

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Experimental program
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Effect test

Embodiment 1

[0019]MRVI1-AS1 increases paclitaxel chemosensitivity in nasopharyngeal carcinoma in vivo and in vitro

[0020] We first performed MTT detection on CNE-1, CNE-1 / T, HNE-2, HNE-2 / T to confirm the paclitaxel resistance of tumor cells ( figure 1 A), and then perform lncRNA chip screening on the above four strains of cells. After screening, we found that the expression of MRVI1-AS1 in the two drug-resistant strains was significantly lower than that of the parental strain ( figure 1 B), MTT results showed that when MRVI1-AS1 was overexpressed in drug-resistant strains, the drug resistance of CNE-1 / T cells to paclitaxel was significantly reversed. Flow cytometry, colony formation and scratch experiments further proved that the overexpression of MRVI1-AS1 can increase the chemotherapy sensitivity of nasopharyngeal carcinoma paclitaxel ( figure 1 C-F). In order to further verify the function of MRVI1-AS1, we subcutaneously injected CNE-1, CNE-1 / T and CNE-1 / T overexpressing MRVI1-AS1 ...

Embodiment 2

[0022] MRVI1-AS1 can increase the chemosensitivity of paclitaxel in nasopharyngeal carcinoma by targeting miR-513a-5p and miR-27b-3p

[0023] In order to further explore the mechanism by which MRVI1-AS1 increases the chemosensitivity of nasopharyngeal carcinoma to paclitaxel, we first determined the intracellular location of MRVI1-AS1 and found that it was expressed in both the nucleus and the cytoplasm ( figure 2 A). Then we performed miRNA and mRNA microarray detection on the three samples of CNE-1, CNE-1 / T and CNE-1 / T+MRVI1-AS1 overexpression strains. In the miRNA microarray, we found that miR-27b-3p and miR- The expression of 513a-5p in the CNE-1 / T+MRVI1-AS1 overexpression strain was significantly lower than that in CNE-1 / T ( figure 2 B), and they also have a possible binding site at the 3'UTR end of MRVI1-AS1 ( figure 2 C). The expression levels of miR-27b-3p and miR-513a-5p were detected in CNE-1 cells and CNE-1 / T cells, and their expression levels in CNE-1 / T cells...

Embodiment 3

[0025] MRVI1-AS1 can increase the chemosensitivity of paclitaxel in nasopharyngeal carcinoma by restoring the expression of ATF3

[0026] In order to further study the downstream target genes of MRVI1-AS1, miR-27b-3p and miR-513a-5p, we analyzed the results of the mRNA chip and combined GEO, TCGA database and miRNA target prediction tool (microRNA.org and TargetScan) , it was found that the expression level of ATF3 after overexpression of MRVI1-AS1 in CNE-1 / T in the chip was significantly rebounded ( Figure 4 A); while the target prediction results show that ATF3 also has binding sites for miR-27b-3p and miR-513a-5p ( Figure 4 B); qRT-PCR results showed that the expression level of ATF3 was significantly increased after overexpressing MRVI1-AS1 in CNE-1 / T cells ( Figure 4 E), and after inhibiting the expression of miR-27b-3p or miR-513a-5p in CNE-1 / T cells, the expression level of ATF3 was also significantly increased ( Figure 4 F). This indicates that miR-513a-5p and m...

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Abstract

The invention discloses application of ATF3 as a target site in preparing a taxol chemosensitization medicine for treating nasopharynx cancer. Tests show that the expression level of an Activating transfactor 3 ATF3 in nasopharynx cancer taxol drug-resistant cells is remarkably lower than that of taxol sensitive cells, and in addition, ATF3 is capable of improving the taxol chemosensitization of nasopharynx cancer by regulating and controlling HIPPO signal paths. Therefore, ATF3 can be used as a potential target site for chemosensitization treatment on nasopharynx cancer. As the target site, ATF3 can be used for preparing nasopharynx cancer chemosensitization treatment medicines, and particularly as the target site, ATF3 can be used for preparing medicines for regulating and controlling HIPPO paths to improve taxol chemosensitization of nasopharyngeal carcinoma cells.

Description

technical field [0001] The invention belongs to the technical field of biomedicine, and specifically relates to the application of ATF3 as a target in the preparation of paclitaxel chemotherapy sensitizing drugs for treating nasopharyngeal carcinoma. Background technique [0002] Nasopharyngeal carcinoma is a type of highly invasive squamous cell carcinoma commonly found in East Asia, Southeast Asia and North Africa. In addition to genetic and environmental factors, Epstein-Barr virus plays an important role in its pathogenesis, which is why it is different from As with other head and neck tumors, nasopharyngeal carcinoma cells have relatively high sensitivity to radiation and the anatomical structure of the head and neck is extremely complex. Therefore, radiotherapy is an extremely effective first-choice treatment for early-stage nasopharyngeal carcinoma patients. According to the latest version of the AJCC (American Joint Commission on Cancer AJCC) staging system, about 60...

Claims

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Application Information

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IPC IPC(8): A61K45/00A61P35/00
CPCA61K45/00A61P35/00
Inventor 曹科何东朱煜星向亮肖梦卿
Owner THE THIRD XIANGYA HOSPITAL OF CENT SOUTH UNIV
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