The mechanism and therapeutic potential of lncRNA MIR497HG/miR-16-5p axis in breast cancer.

Quan Cheng, Dong-Yang Yu, Yong-Hong Zhou, Jian-Yuan Huang
Author Information
  1. Quan Cheng: Department of Chinese Medicine, Hangzhou First People's Hospital, Hangzhou, 310006, China.
  2. Dong-Yang Yu: Department of Urology, People's Hospital of Yilong County, Nanchong, 637600, China.
  3. Yong-Hong Zhou: Department of General Surgery (Thyroid Gland/Blood Vessel), The First People's Hospital of Neijiang, No. 1866, West Section of Han'an Avenue, Neijiang, 641099, China.
  4. Jian-Yuan Huang: Department of General Surgery (Thyroid Gland/Blood Vessel), The First People's Hospital of Neijiang, No. 1866, West Section of Han'an Avenue, Neijiang, 641099, China. huangjianyuan7388@163.com.

Abstract

BACKGROUND: Breast cancer has become a major public health problem in the current society, and its incidence rate ranks the first among Chinese female malignant tumors. This paper once again confirmed the efficacy of lncRNA in tumor regulation by introducing the mechanism of the diagnosis of breast cancer by the MIR497HG/miR-16-5p axis.
METHODS: The abnormal expression of MIR497HG in breast cancer was determined by RT-qPCR method, and the correlation between MIR497HG expression and clinicopathological characteristics of breast cancer patients was analyzed via Chi-square test. To understand the diagnostic potential of MIR497HG in breast cancer by drawing the receiver operating characteristic curve (ROC). The overexpressed MIR497HG (pcDNA3.1-MIR497HG) was designed and constructed to explore the regulation of elevated MIR497HG on biological function of BT549 and Hs 578T cells through Transwell assays. Additionally, the luciferase gene reporter assay and Pearson analysis evaluated the targeting relationship of MIR497HG to miR-16-5p.
RESULTS: MIR497HG was decreased in breast cancer and had high diagnostic function, while elevated MIR497HG inhibited the migration and invasion of BT549 and Hs 578T cells. In terms of functional mechanism, miR-16-5p was the target of MIR497HG, and MIR497HG reversely regulated the miR-16-5p. miR-16-5p mimic reversed the effects of upregulated MIR497HG on cell biological function.
CONCLUSIONS: In general, MIR497HG was decreased in breast cancer, and the MIR497HG/miR-16-5p axis regulated breast cancer tumorigenesis, providing effective insights for the diagnosis of patients.

Keywords

References

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MeSH Term

Humans
MicroRNAs
Female
Breast Neoplasms
RNA, Long Noncoding
Cell Line, Tumor
Gene Expression Regulation, Neoplastic
Cell Movement
Middle Aged
Cell Proliferation

Chemicals

MicroRNAs
RNA, Long Noncoding
MIRN16 microRNA, human

Word Cloud

Created with Highcharts 10.0.0MIR497HGcancerbreastmiR-16-5plncRNAmechanismMIR497HG/miR-16-5paxisfunctionBreastregulationdiagnosisexpressionpatientsdiagnosticpotentialelevatedbiologicalBT549Hs578TcellsregulatedBACKGROUND:becomemajorpublichealthproblemcurrentsocietyincidencerateranksfirstamongChinesefemalemalignanttumorspaperconfirmedefficacytumorintroducingMETHODS:abnormaldeterminedRT-qPCRmethodcorrelationclinicopathologicalcharacteristicsanalyzedviaChi-squaretestunderstanddrawingreceiveroperatingcharacteristiccurveROCoverexpressedpcDNA31-MIR497HGdesignedconstructedexploreTranswellassaysAdditionallyluciferasegenereporterassay andPearsonanalysisevaluatedtargetingrelationshipRESULTS:decreasedhighinhibitedmigrationinvasiontermsfunctionaltargetreverselymimicreversedeffectsupregulatedcellCONCLUSIONS:generalwas decreasedtumorigenesisprovidingeffectiveinsightstherapeuticDiagnosisInvasionMigration

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