Electronic Journal of Liver Tumor ›› 2021, Vol. 8 ›› Issue (2): 26-32.

• Original article • Previous Articles     Next Articles

lncRNA MALAT1 impacts cholangiocarcinoma initiation and development by regulating RBE cell invasion and apoptosis

Wei Zhicheng1, Ma Teng1, Che Xu1,2, Zhao Hong3,*   

  1. 1. Department of Hepatobiliary Surgery, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital & Shenzhen Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Shenzhen 518116, Guangdong, China;
    2. Department of Pancreatic and Gastric Surgery, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China;
    3. Department of Hepatobiliary Surgery, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China
  • Received:2021-03-29 Published:2021-07-16

Abstract: Objective: This study aims to explore that metastasis associated in lung denocarcinoma transcript 1(MALAT1)participates in intrahepatic cholangiocarcinoma (ICC) initiation and development via regulating cell invasion, migration, apoptosis in vitro and cell proliferation in vivo. Methods: GeneCards and LncExpDB database were used to reveal basic information of MALAT1. qRT-PCR and FISH were used to detect MALAT1 expression in 27 cases of ICC. Tranwell, Cell wound scratch and Tunel cell apoptosis were used to detect impacts of MALAT1 on RBE cell invasion, migration and apoptosis. FISH, PCNA immunohistochemistry and Ki67 Immunofluorescence were used to detect fluorescent probe signal of MALAT1 in subcutaneous tumor tissues and the cell proliferation in vivo. Results: MALAT1 located in 11p13.1 with a length of 8708bp in transcript, showing different expression in multiple tumors and diseases. MALAT1 was up-regulated in 27 cases of ICC. MALAT1 promoted RBE cell invasion, migration and inhibited apoptosis, while knockdown of MALAT1 could facilitate apoptosis. Positive expression of MALAT1 in subcutaneous tumor tissues was obviously increased. Over-expression MALAT1 could promote in vivo cell proliferation, whereas knockdown of MALAT1 could inhibit in vivo cell proliferation. Conclusion: MALAT1 could serve as a potential maker in ICC, and siMALAT1 provides new studying directions for cholangiocarcinoma diagnosis and therapies.

Key words: Cholangiocarcinoma, Metastasis associated in lung denocarcinoma transcript 1, Small interfering RNA, Human bile duct carcinoma cell