Long non-coding RNA LINC00346 promotes pancreatic cancer growth and gemcitabine resistance by sponging miR-188-3p to derepress BRD4 expression View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2019-02-06

AUTHORS

Weidong Shi, Chenyue Zhang, Zhouyu Ning, Yongqiang Hua, Ye Li, Lianyu Chen, Luming Liu, Zhen Chen, Zhiqiang Meng

ABSTRACT

BACKGROUND: Long non-coding RNA LINC00346 has been recently suggested as a prognostic marker in pancreatic cancer. However, its biological function in pancreatic cancer has not yet been determined. In this study, we attempted to ascertain the role of LINC00346 in regulating the aggressiveness of pancreatic cancer. METHODS: The effects of overexpression and knockdown of LINC00346 on the proliferation, cell cycle progression, apoptosis, and gemcitabine resistance were investigated. Bioinformatic analysis, luciferase reporter assay, and RNA immunoprecipitation assay were performed to search for potential microRNAs (miRs) that can interact with LINC00346. RESULTS: Overexpression of LINC00346 significantly enhanced the proliferation, colony formation, and tumorigenesis of pancreatic cancer cells. Conversely, knockdown of LINC00346 suppressed pancreatic cancer cell proliferation and caused a cell-cycle arrest at the G2/M-phase. Depletion of LINC00346 also enhanced gemcitabine sensitivity in pancreatic cancer cells both in vitro and in vivo. Mechanistic investigation revealed that LINC00346 acted as a sponge for miR-188-3p and blocked the repression of BRD4 by miR-188-3p in pancreatic cancer cells. Clinical evidence indicated a negative correlation between LINC00346 and miR-188-3p in pancreatic cancer specimens. Rescue experiments showed that LINC00346 attenuated the growth-suppressing and chemosensitizing effects of miR-188-3p on pancreatic cancer cells. In addition, silencing of BRD4 significantly inhibited LINC00346-induced pancreatic cancer cell proliferation and colony formation. CONCLUSIONS: LINC00346 shows the ability to promote pancreatic cancer growth and gemcitabine resistance, which is in part mediated by antagonization of miR-188-3p and induction of BRD4. Targeting LINC00346 may improve gemcitabine-based therapeutic efficacy. More... »

PAGES

60

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/s13046-019-1055-9

DOI

http://dx.doi.org/10.1186/s13046-019-1055-9

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https://app.dimensions.ai/details/publication/pub.1111954587

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/30728036


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29 schema:description BACKGROUND: Long non-coding RNA LINC00346 has been recently suggested as a prognostic marker in pancreatic cancer. However, its biological function in pancreatic cancer has not yet been determined. In this study, we attempted to ascertain the role of LINC00346 in regulating the aggressiveness of pancreatic cancer. METHODS: The effects of overexpression and knockdown of LINC00346 on the proliferation, cell cycle progression, apoptosis, and gemcitabine resistance were investigated. Bioinformatic analysis, luciferase reporter assay, and RNA immunoprecipitation assay were performed to search for potential microRNAs (miRs) that can interact with LINC00346. RESULTS: Overexpression of LINC00346 significantly enhanced the proliferation, colony formation, and tumorigenesis of pancreatic cancer cells. Conversely, knockdown of LINC00346 suppressed pancreatic cancer cell proliferation and caused a cell-cycle arrest at the G2/M-phase. Depletion of LINC00346 also enhanced gemcitabine sensitivity in pancreatic cancer cells both in vitro and in vivo. Mechanistic investigation revealed that LINC00346 acted as a sponge for miR-188-3p and blocked the repression of BRD4 by miR-188-3p in pancreatic cancer cells. Clinical evidence indicated a negative correlation between LINC00346 and miR-188-3p in pancreatic cancer specimens. Rescue experiments showed that LINC00346 attenuated the growth-suppressing and chemosensitizing effects of miR-188-3p on pancreatic cancer cells. In addition, silencing of BRD4 significantly inhibited LINC00346-induced pancreatic cancer cell proliferation and colony formation. CONCLUSIONS: LINC00346 shows the ability to promote pancreatic cancer growth and gemcitabine resistance, which is in part mediated by antagonization of miR-188-3p and induction of BRD4. Targeting LINC00346 may improve gemcitabine-based therapeutic efficacy.
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36 schema:keywords BRD4
37 BRD4 expression
38 Depletion of LINC00346
39 G2/M
40 LINC00346
41 LINC00346-induced pancreatic cancer cell proliferation
42 Long non-coding RNA LINC00346
43 Mechanistic investigations
44 Overexpression of LINC00346
45 RNA LINC00346
46 RNA immunoprecipitation
47 ability
48 addition
49 aggressiveness
50 analysis
51 antagonization
52 apoptosis
53 arrest
54 bioinformatics analysis
55 biological functions
56 cancer
57 cancer cell proliferation
58 cancer cells
59 cancer growth
60 cancer specimens
61 cell cycle arrest
62 cell cycle progression
63 cell proliferation
64 cells
65 clinical evidence
66 colony formation
67 correlation
68 cycle progression
69 depletion
70 effect
71 effects of overexpression
72 efficacy
73 evidence
74 experiments
75 expression
76 formation
77 function
78 gemcitabine resistance
79 gemcitabine sensitivity
80 gemcitabine-based therapeutic efficacy
81 growth
82 immunoprecipitation
83 induction
84 induction of BRD4
85 investigation
86 knockdown
87 knockdown of LINC00346
88 luciferase reporter
89 markers
90 microRNAs
91 negative correlation
92 non-coding RNA LINC00346
93 overexpression
94 pancreatic cancer
95 pancreatic cancer cell proliferation
96 pancreatic cancer cells
97 pancreatic cancer growth
98 pancreatic cancer specimens
99 part
100 phase
101 potential microRNAs
102 prognostic marker
103 progression
104 proliferation
105 reporter
106 repression
107 repression of BRD4
108 rescue experiments
109 resistance
110 role
111 role of LINC00346
112 sensitivity
113 specimens
114 sponges
115 study
116 therapeutic efficacy
117 tumorigenesis
118 vivo
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