miR-874 inhibits gastric cancer cell proliferation by targeting SPAG9.
Adaptor Proteins, Signal Transducing
/ genetics
Adult
Aged
Animals
Apoptosis
/ drug effects
Cell Line, Tumor
Cell Proliferation
/ drug effects
Down-Regulation
Female
Gastric Mucosa
/ cytology
Gene Expression Regulation, Neoplastic
Humans
Male
Mice
MicroRNAs
/ agonists
Middle Aged
Stomach Neoplasms
/ genetics
Xenograft Model Antitumor Assays
Apoptosis
Gastric cancer
Proliferation
SPAG9
miR-874
Journal
BMC cancer
ISSN: 1471-2407
Titre abrégé: BMC Cancer
Pays: England
ID NLM: 100967800
Informations de publication
Date de publication:
05 Jun 2020
05 Jun 2020
Historique:
received:
13
02
2020
accepted:
22
05
2020
entrez:
7
6
2020
pubmed:
7
6
2020
medline:
20
1
2021
Statut:
epublish
Résumé
microRNAs (miRNAs) play essential roles in the development and progression of gastric cancer (GC). Although aberrant miR-874 expression has been reported in various human cancers, its role in GC remains obscure. miR-874 expression was assessed by real-time quantitative polymerase chain reaction (RT-qPCR) in 62 matched GC and adjacent normal tissues, as well as in GC cell lines and immortalized human gastric epithelial cells. CCK8 assay, colony formation assay, and flow cytometry were used to assess the role of miR-874 in GC cell proliferation and apoptosis in vitro. Additionally, to determine the effects of miR-874 on GC cell proliferation and apoptosis in vivo, BALB/c nude mice were injected with GC cells transfected with a miR-874 mimic. The role of miR-874 in SPAG9 expression was assessed by luciferase assay, Western blotting, and RT-qPCR. miR-874 was downregulated in GC cell lines and tissues. miR-874 overexpression in GC cells led to inhibition of cell proliferation and induction of apoptosis. Moreover, SPAG9 was identified as a direct miR-874 target, the expression of which was suppressed by miR-874. SPAG9 overexpression markedly promoted GC cell proliferation. miR-874 inhibited cell proliferation and induced apoptosis in GC cells. SPAG9 downregulation was crucial for the tumor-suppressive effects of miR-874. Hence, the miR-874/SPAG9 axis could serve as a novel therapeutic target in GC.
Sections du résumé
BACKGROUND
BACKGROUND
microRNAs (miRNAs) play essential roles in the development and progression of gastric cancer (GC). Although aberrant miR-874 expression has been reported in various human cancers, its role in GC remains obscure.
METHODS
METHODS
miR-874 expression was assessed by real-time quantitative polymerase chain reaction (RT-qPCR) in 62 matched GC and adjacent normal tissues, as well as in GC cell lines and immortalized human gastric epithelial cells. CCK8 assay, colony formation assay, and flow cytometry were used to assess the role of miR-874 in GC cell proliferation and apoptosis in vitro. Additionally, to determine the effects of miR-874 on GC cell proliferation and apoptosis in vivo, BALB/c nude mice were injected with GC cells transfected with a miR-874 mimic. The role of miR-874 in SPAG9 expression was assessed by luciferase assay, Western blotting, and RT-qPCR.
RESULTS
RESULTS
miR-874 was downregulated in GC cell lines and tissues. miR-874 overexpression in GC cells led to inhibition of cell proliferation and induction of apoptosis. Moreover, SPAG9 was identified as a direct miR-874 target, the expression of which was suppressed by miR-874. SPAG9 overexpression markedly promoted GC cell proliferation.
CONCLUSIONS
CONCLUSIONS
miR-874 inhibited cell proliferation and induced apoptosis in GC cells. SPAG9 downregulation was crucial for the tumor-suppressive effects of miR-874. Hence, the miR-874/SPAG9 axis could serve as a novel therapeutic target in GC.
Identifiants
pubmed: 32503577
doi: 10.1186/s12885-020-06994-z
pii: 10.1186/s12885-020-06994-z
pmc: PMC7275545
doi:
Substances chimiques
Adaptor Proteins, Signal Transducing
0
MIRN874 microRNA, human
0
MicroRNAs
0
SPAG9 protein, human
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
522Références
Am J Cancer Res. 2017 Jun 01;7(6):1310-1321
pubmed: 28670493
J Cell Commun Signal. 2020 Jun;14(2):193-205
pubmed: 32067207
United European Gastroenterol J. 2020 Mar;8(2):140-147
pubmed: 32213066
Thorac Cancer. 2020 Jun;11(6):1550-1558
pubmed: 32301290
Eur Rev Med Pharmacol Sci. 2019 May;23(9):3779-3789
pubmed: 31115004
Cancer Cell Int. 2020 Feb 19;20:57
pubmed: 32099530
Int J Mol Sci. 2020 Jan 29;21(3):
pubmed: 32013265
Eur Rev Med Pharmacol Sci. 2018 Jun;22(12):3812-3818
pubmed: 29949157
Eur Rev Med Pharmacol Sci. 2020 Jan;24(2):664-672
pubmed: 32016967
Tumour Biol. 2014 Jul;35(7):6949-54
pubmed: 24740566
Gut Pathog. 2020 Apr 24;12:23
pubmed: 32346400
PLoS One. 2020 Apr 29;15(4):e0232429
pubmed: 32348353
Panminerva Med. 2019 Jul 25;:
pubmed: 31352763
Mol Cell Endocrinol. 2014 Jun 5;390(1-2):73-84
pubmed: 24747602
J Cancer. 2020 Mar 13;11(12):3483-3491
pubmed: 32284744
Mol Med Rep. 2019 Mar;19(3):1926-1934
pubmed: 30628682
Cell Prolif. 2019 May;52(3):e12567
pubmed: 30883979
Biochem Biophys Res Commun. 2016 Feb 12;470(3):620-626
pubmed: 26797273
Anticancer Drugs. 2019 Sep;30(8):803-811
pubmed: 31419217
Biosci Rep. 2019 Sep 3;39(9):
pubmed: 31416884
Onco Targets Ther. 2019 Jun 21;12:4927-4936
pubmed: 31417287
EBioMedicine. 2019 Jul;45:181-191
pubmed: 31248836
Biol Chem. 2019 Jul 9;:
pubmed: 31287793
Am J Transl Res. 2019 Aug 15;11(8):5249-5260
pubmed: 31497238
Am J Cancer Res. 2018 Dec 01;8(12):2467-2480
pubmed: 30662804