Abstract:Cervical cancer is a common gynecological malignancy with high morbidity worldwide. MicroRNAs (miRNAs) serve critical roles in cervical cancer progression. Accumulating evidence indicates that miR-873 functions as a tumor suppressor in certain types of cancer. However, the function and mechanism of miR-873 in the progression of cervical cancer have not been completely elucidated. In the present study, the role and mechanism of miR-873 in the proliferation, migration and invasion of cervical cancer cells were i… Show more
“…20 MiR-873 can suppress the viability of CC cells, thus retarding the development of CC. 21 In addition, miR-128 has been reported to play an anti-cancer role in CC. 22 A recent study has showed that up-regulation of miR-128 conspicuously inhibits the cell viability and epithelial-mesenchymal transition (EMT) procession in CC.…”
Long non-coding RNAs (lncRNAs) play major roles in the development of several cancers, including cervical cancer (CC). The purpose of the present study is to explore the regulatory mechanism of MIR4435-2HG on CC in vitro. Patients and Methods: Fifty-nine pairs of CC tissues and adjacent normal tissues were collected from 59 patients by resection. The expression of lncRNA MIR4435-2HG, microRNA (miR)-128-3p and Musashi 2 (MSI2) in CC tissues and cells was detected by quantitative reverse-transcription PCR (qRT-PCR). The viability of CC cells was detected by 3-(4, 5-Dimethyl-2-Thiazolyl)-2, 5-Diphenyl-2-H-Tetrazolium Bromide (MTT) assay. The ability of migration and invasion in CC cells was measured by wound healing assay and transwell invasion assay, respectively. Starbase software and Targetscan software were utilized to predict the relationship between miR-128 and MIR4435-2HG/MSI2, respectively. The dual-luciferase reporter assay was used to confirm these interactions. Results: LncRNA MIR4435-2HG expression was significantly up-regulated in CC tissues (P < 0.001) and cells (P < 0.01). Knockdown of MIR4435-2HG inhibited the proliferation, migration and invasion of CC cells (P < 0.01). MiR-128-3p was a target of MIR4435-2HG and was negatively modulated by MIR4435-2HG (P < 0.0001, r = −0.6331). Up-regulation of miR-128-3p suppressed the proliferation, migration and invasion of CC cells (P < 0.01). In addition, MSI2 was the target gene of miR-128-3p and negatively regulated by miR-128-3p (P < 0.0001, r = −0.4775). Both down-regulation of miR-128-3p and up-regulation of MSI2 reversed the inhibitory effects of MIR4435-2HG knockdown on the proliferation, migration and invasion of CC cells (P < 0.05). Conclusion: MIR4435-2HG knockdown suppresses the proliferation, migration and invasion of CC cells through regulating the miR-128-3p/MSI2 axis, providing a possible therapeutic strategy for CC.
“…20 MiR-873 can suppress the viability of CC cells, thus retarding the development of CC. 21 In addition, miR-128 has been reported to play an anti-cancer role in CC. 22 A recent study has showed that up-regulation of miR-128 conspicuously inhibits the cell viability and epithelial-mesenchymal transition (EMT) procession in CC.…”
Long non-coding RNAs (lncRNAs) play major roles in the development of several cancers, including cervical cancer (CC). The purpose of the present study is to explore the regulatory mechanism of MIR4435-2HG on CC in vitro. Patients and Methods: Fifty-nine pairs of CC tissues and adjacent normal tissues were collected from 59 patients by resection. The expression of lncRNA MIR4435-2HG, microRNA (miR)-128-3p and Musashi 2 (MSI2) in CC tissues and cells was detected by quantitative reverse-transcription PCR (qRT-PCR). The viability of CC cells was detected by 3-(4, 5-Dimethyl-2-Thiazolyl)-2, 5-Diphenyl-2-H-Tetrazolium Bromide (MTT) assay. The ability of migration and invasion in CC cells was measured by wound healing assay and transwell invasion assay, respectively. Starbase software and Targetscan software were utilized to predict the relationship between miR-128 and MIR4435-2HG/MSI2, respectively. The dual-luciferase reporter assay was used to confirm these interactions. Results: LncRNA MIR4435-2HG expression was significantly up-regulated in CC tissues (P < 0.001) and cells (P < 0.01). Knockdown of MIR4435-2HG inhibited the proliferation, migration and invasion of CC cells (P < 0.01). MiR-128-3p was a target of MIR4435-2HG and was negatively modulated by MIR4435-2HG (P < 0.0001, r = −0.6331). Up-regulation of miR-128-3p suppressed the proliferation, migration and invasion of CC cells (P < 0.01). In addition, MSI2 was the target gene of miR-128-3p and negatively regulated by miR-128-3p (P < 0.0001, r = −0.4775). Both down-regulation of miR-128-3p and up-regulation of MSI2 reversed the inhibitory effects of MIR4435-2HG knockdown on the proliferation, migration and invasion of CC cells (P < 0.05). Conclusion: MIR4435-2HG knockdown suppresses the proliferation, migration and invasion of CC cells through regulating the miR-128-3p/MSI2 axis, providing a possible therapeutic strategy for CC.
“…A bioinformatics analysis revealed a total of 22 miRNAs that were capable of complementary base pairing with LINC01426 ( Figure 3C ). Among these candidates, miR-519d-5p, 29 miR-873-3p, 30 , 31 miR-377-5p, 32 , 33 and miR-548c-3p 34 , 35 were selected for experimental verification because they played critical functions in various human cancers. Figure 3 LINC01426 is a molecular sponge for miR-519d-5p in NSCLC cells.…”
Purpose
Recent studies have identified important roles for
long intergenic non-protein coding RNA 1426
(
LINC01426
) in glioma and clear cell renal cell carcinoma. The present study evaluated the expression profile of
LINC01426
in non-small cell lung cancer (NSCLC) tissues and cell lines. Furthermore, the function of
LINC01426
in NSCLC and the molecular mechanisms involved were extensively studied.
Methods
The abundance of
LINC01426
in NSCLC tissues and cell lines was determined using quantitative reverse transcription–polymerase chain reaction. The cell counting kit-8 assay, flow cytometry, transwell experiments for migration and invasion, and xenograft tumor model were used to assess the function of
LINC01426
in NSCLC cells. Mechanistic studies were performed using the luciferase reporter assay and RNA immunoprecipitation.
Results
Significant
LINC01426
upregulation was observed in NSCLC tissues and cell lines. Silencing
LINC01426
inhibited proliferation, migration, and invasion of NSCLC cells and facilitated cell apoptosis in vitro. Furthermore, interference of
LINC01426
restricted tumor growth of NSCLC cells in vivo. In addition,
LINC01426
showed the ability to directly bind to microRNA-519d-5p (miR-519d-5p) and act as a molecular sponge for miR-519d-5p in NSCLC cells. Furthermore, the
ETS proto-oncogene 1
(
ETS1
) was identified as a direct target of miR-519d-5p and
LINC01426
could indirectly upregulate
ETS1
expression by sponging miR-519d-5p. Moreover, the cancer-inhibiting activities of
LINC01426
knockdown in NSCLC cells were partially offset by miR-519d-5p inhibition.
Conclusion
LINC01426
increases
ETS1
expression by sequestering miR-519d-5p, thereby aggravating the malignant progression of NSCLC. The LINC01426/miR-519d-5p/ETS1 competing endogenous RNA pathway may provide a target for designing therapeutic agents for NSCLC treatment.
Section: Mir-873-5p Dysregulation In Various Cancersmentioning
confidence: 99%
“…GLI1 is a transcription factor of the Hh signaling pathway and downstream target genes and is usually used as a marker to activate the Hh signaling pathway ( 80 ). Studies have found that increased expression of miR-873-5p can inhibit the expression of GLI1 and inhibit the cell proliferation of NSCLC ( 4 ), GC ( 51 ), and CC ( 35 ) through the Hh signaling pathway. STRA6, as a transmembrane protein of RA, is overexpressed in many cancer types ( 81 ).…”
Section: The Biological Role Of Mir-873-5p In Human Cancermentioning
confidence: 99%
“…When miR-873-5p targets to inhibit GLI1, the expression level of E-cadherin is significantly increased, while the levels of N-cadherin and vimentin are significantly reduced, thereby inhibiting the EMT process of CC cells ( 35 ). miR-873-5p can negatively regulate ULBP2 and activate immune cells, thereby reducing the invasion and metastasis of CC cells ( 34 ).…”
Section: The Biological Role Of Mir-873-5p In Human Cancermentioning
miR-873 is a microRNA located on chromosome 9p21.1. miR-873-5p and miR-873-3p are the two main members of the miR-873 family. Most studies focus on miR-873-5p, and there are a few studies on miR-873-3p. The expression level of miR-873-5p was down-regulated in 14 cancers and up-regulated in 4 cancers. miR-873-5p has many targeted genes, which have unique molecular functions such as catalytic activity, transcription regulation, and binding. miR-873-5p affects cancer development through the PIK3/AKT/mTOR, Wnt/β-Catenin, NF-κβ, and MEK/ERK signaling pathways. In addition, the target genes of miR-873-5p are closely related to the proliferation, apoptosis, migration, invasion, cell cycle, cell stemness, and glycolysis of cancer cells. The target genes of miR-873-5p are also related to the efficacy of several anti-cancer drugs. Currently, in cancer, the expression of miR-873-5p is regulated by a variety of epigenetic factors. This review summarizes the role and mechanism of miR-873-5p in human tumors shows the potential value of miR-873-5p as a molecular marker for cancer diagnosis and prognosis.
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