miR‑331‑3p suppresses cell invasion and migration in colorectal carcinoma by directly targeting NRP2

Zhang, Hongye; Wang, Ruiyu; Wang, Mingxia

doi:10.3892/ol.2019.11029

Cited by 20 publications

(22 citation statements)

References 35 publications

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“…CRC is a fatal illness with high mortality and morbidity (35), and high rates of metastasis and recurrence (6). Despite the use of surgical and adjuvant therapy, the survival rate has not improved dramatically, and ~50% of patients die from local recurrence or metastasis following surgery (36). Novel biomarkers and effective therapeutic targets are urgently required.…”

Section: Discussionmentioning

confidence: 99%

Hsa_circ_0038646 promotes cell proliferation and migration in colorectal cancer via miR‑331‑3p/GRIK3

Zhou

Chen

et al. 2020

Oncol Lett

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Increasing evidence supports the essential roles of circular RNAs (circRNAs) and microRNAs (miRNAs/miRs) in different types of human cancer. For example, hsa_ circ_0137008 functions as a sponge for mi-338-5p and inhibits the malignant phenotype in colorectal cancer. Furthermore, hsa_circ_RNA_0011780 downregulates FBXW7 by targeting miR-554a and suppressing the progression of non-small cell lung cancer. Thus far, only a single report has identified that the miRNA miR-331-3p exerts a pivotal effect on human colorectal cancer (CRC) evolution. However, both the upand downstream regulatory mechanisms of miR-331-3p are unclear. In the present study, it was predicted via bioinformatics analysis that the circRNA, hsa_circ_0038646, and the glutamate receptor ionotropic kainate 3 (GRIK3) gene contain binding sites that can interact with miR-331-3p. Thus, hsa_ circ_0038646/miR-331-3p/GRIK3 may be a novel therapeutic pathway for CRC. Reverse transcription-quantitative PCR and western blotting analyses were performed, as well as cell proliferation, luciferase reporter and Transwell migration assays. Hsa_circ_0038646 was overexpressed in both CRC cells and tissues, and this aberrant expression was positively related with increasing tumor grade. Knockdown of hsa_circ_0038646 significantly weakened human CRC cell proliferation and migration. It was shown that hsa_circ_0038646 can sponge miR-331-3p to suppress its expression, and that suppression of miR-331-3p can reverse the effects of hsa_circ_0038646 inhibition in CRC cells. It was determined that GRIK3 is a downstream target of miR-331-3p, and that hsa_circ_0038646 could increase the levels of GRIK3 by suppressing miR-331-3p in CRC cells. Restoring GRIK3 expression rescued the weakened CRC cell proliferation and migration following hsa_circ_0038646 knockdown. The present study indicated that hsa_circ_0038646 functions as a tumor promoter in CRC by increasing GRIK3 expression via sponging of miR-331-3p. The hsa_circ_0038646/miR-331-3p/GRIK3 axis may be a novel therapeutic and diagnostic target of CRC.

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Section: Discussionmentioning

confidence: 99%

Hsa_circ_0038646 promotes cell proliferation and migration in colorectal cancer via miR‑331‑3p/GRIK3

Zhou

Chen

et al. 2020

Oncol Lett

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“…For example, MIR-17-5p and MIR-20a are both highly expressed in colon cancer tissues, and the MIR-106 family was also found to be closely involved in the initiation and development of colorectal cancer [ 31 , 32 ]. On the contrary, the miRNA target of IRF7, MIR-331, was reported to be a tumor suppressor in colorectal carcinoma [ 33 ].…”

Section: Discussionmentioning

confidence: 99%

Identification of the Prognostic Value and Clinical Significance of Interferon Regulatory Factors (IRFs) in Colon Adenocarcinoma

Yuemaier

Zhou

et al. 2020

Med Sci Monit

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“…Besides, we found miR-331 was a new miRNA which has not been reported in transmission of drug resistance. It has been reported that miR-331-3p could inhibit the proliferation and migration of colon cancer by targeting NRP2 18 .Another study showed that circ-0001649 sponges with miR-331-3p, further to achieve inhibition of miR-331-3p so that the biological process of non-small cell lung cancer was suppressed 19 .The high expression of miR-331-3p in serum was considered to be one of the high risk factors for esophageal cancer recurrence.Studies related to miR-331 and chemotherapy in leukemia have shown that the increased expression of miR-331 may lead to poor e cacy and lower survival rate 20 .The above studies have shown that miR-331-3p can cause tumor recurrence and poor prognosis in some tumors. In conclusion, we found that the regulatory role of miR-331 in different tumors is not uniform.…”

Section: Mir-331 Carried By Exosomes Could Promote the Autophagy To Induce Drug Resistance In Osmentioning

confidence: 99%

Exosomal miR-331 from Chemoresistant Osteosarcoma Cells Induced Chemoresistance Through Autophagy

Zhao¹,

Zhao²,

Liu

et al. 2021

Preprint

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Background Osteosarcoma (OS) is a highly malignant tumor. Improving chemotherapeutic resistance is very important to improve the survival rate of OS. Exosomes and microRNAs (MiRNA) play important roles in the mechanism of chemotherapeutic resistance transmission. More and more researches focus the mechanism of miRNAs carried by exosomes in the transmission of chemotherapeutic resistance of OS. This study focused on exploring the mechanism of exosomal miR-331 in the transmission of chemoresistance in OS. Methods We cultured OS drug-resistant cells and extracted exosomes of these cells. The secretion and uptake of exosomes in OS drug-resistant cells and OS cells (OSCs) were confirmed by fluorescence tracking assay and transwell experiments. The differential expression of microRNA-331 (miR-331) in exosomes of OS resistant and OS cells was investigated by RT-PCR. The effects of drug-resistant exosomes on proliferation and migration of OS cells were determined by MTT assay and scratches assay. MDC staining, RT-PCR, and Western blot were used to detect the role of autophagy which regulated by drug-resistant cell-derived exosom-miR-331. Results We found that the expression difference of miR-331 between drug-resistant cells of MG63 and HOS cell lines and tumor cells was the most significant. Drug resistant OSCs secreted exosomes and were ingested by OSCs, which then promoted OSCs to acquire drug resistance. In addition, exosomes secreted by drug-resistant OSCs promote drug resistance by carrying miRNAs. Interestingly, inhibition of miRNA resulted in reduced drug resistance transmission of exosomes. Finally, we found that the exosomes secreted by drug-resistant OSCs could induce autophagy of OSCs by carrying miR-331, thus making OSCs acquire drug resistance. Inhibition of miR-331 can effectively improve drug resistance of OSCs. Conclusions Chemoresistant OSCs-derived exosomes promote the transmission of drug resistance by carrying miR-331 and inducing autophagy. Inhibition of miR-331 could effectively alleviate drug resistance of OSCs.

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miR‑331‑3p suppresses cell invasion and migration in colorectal carcinoma by directly targeting NRP2

Cited by 20 publications

References 35 publications

Hsa_circ_0038646 promotes cell proliferation and migration in colorectal cancer via miR‑331‑3p/GRIK3

Hsa_circ_0038646 promotes cell proliferation and migration in colorectal cancer via miR‑331‑3p/GRIK3

Identification of the Prognostic Value and Clinical Significance of Interferon Regulatory Factors (IRFs) in Colon Adenocarcinoma

Exosomal miR-331 from Chemoresistant Osteosarcoma Cells Induced Chemoresistance Through Autophagy

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