MAGI2‐AS3 suppresses MYC signaling to inhibit cell proliferation and migration in ovarian cancer through targeting miR‐525‐5p/MXD1 axis

Autor: Baixue Li, Xue Zhang, Xiangkai Meng, Hua Chang
Jazyk: angličtina
Rok vydání: 2020
Předmět:
0301 basic medicine
Cancer Research
Biology
lcsh:RC254-282
Proto-Oncogene Proteins c-myc
03 medical and health sciences
0302 clinical medicine
Molecular level
Cell Movement
Cell Line
Tumor
miR‐525‐5p
medicine
MXD1
Humans
Radiology
Nuclear Medicine and imaging
Neoplasm Invasiveness
Original Research
Cancer Biology
Adaptor Proteins
Signal Transducing
Cell Proliferation
Ovarian Neoplasms
Cell growth
Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
Advanced stage
Cell Cycle
RNA
Cell cycle
medicine.disease
lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens
Repressor Proteins
MicroRNAs
030104 developmental biology
MAGI2‐AS3
ovarian cancer
Oncology
Apoptosis
030220 oncology & carcinogenesis
Cancer research
Disease Progression
Female
Ovarian cancer
Guanylate Kinases
Zdroj: Cancer Medicine, Vol 9, Iss 17, Pp 6377-6386 (2020)
Cancer Medicine
ISSN: 2045-7634
Popis: Ovarian cancer (OV) is one of the most lethal gynecological malignance in females, and usually diagnosed at advanced stages. Long noncoding RNAs (lncRNAs) exhibit their crucial functions in modulatory mechanisms of cancers. Substantive studies have proven the anti‐tumor role of MAGI2‐AS3 in multiple cancers, but the physiological functions of MAGI2‐AS3 in OV need more detailed explanations. The current study corroborated that overexpression of MAGI2‐AS3 executed inhibitory activity in OV via hindering cell proliferation, cell cycle, migration as well as invasion while promoted apoptosis. Moreover MAGI2‐AS3 bound with miR‐525‐5p and negatively regulated the expression of miR‐525‐5p. Further studies testified that MXD1 was a downstream target of miR‐525‐5p and the competing relationship between MAGI2‐AS3 and MXD1 were confirmed by RNA pull down. Based on the combination between MAX and MYC, we analyzed the effects of MAGI2‐AS3 on MXD1 and MYC, unveiling the competing relationship between MXD1 and MYC for binding to MAX. Finally, we constructed rescue assays to certify that MAGI2‐AS3 suppressed the course of OV via enhancing MXD1 expression. In summary, MAGI2‐AS3 repressed the progression of OV by targeting miR‐525‐5p/MXD1 axis, offering a novel insight into understanding OV at the molecular level.
Overexpression of MAGI2‐AS3 obstructed proliferation and motility in Ovarian cancer (OV) cells. MAGI2‐AS3 modulated the expression of miR‐525‐5p via binding to it. MXD1 was a downstream target of miR‐525‐5p in OV. MXD1 bound with MAX to repress the combination between MAX and MYC. MAGI2‐AS3 suppressed the growth of OV by elevating MXD1 expression.
Databáze: OpenAIRE
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