MiRNA-338-3p regulates cervical cancer cells proliferation by targeting MACC1 through MAPK signaling pathway

Eur Rev Med Pharmacol Sci. 2017 Dec;21(23):5342-5352. doi: 10.26355/eurrev_201712_13919.


Objective: Aberrant expression of miR-338-3p has recently involved in the progression and development of various types of malignant tumors, but its role in the progression of cervical cancer remains unknown. This study aims to investigate the role of miR-338-3p/MACC1 axis in the progression of cervical cancer.

Patients and methods: MiR-338-3p and metastasis-associated in colon cancer 1 (MACC1) expression was determined in cervical cancer by quantitative real-time PCR (qRT-PCR). We explored the association of miR-338-3p expression with pathology and prognosis in cervical cancer patients. We explored the function of miR-338-3p and MACC1 on cell proliferation. A luciferase reporter assay was conducted to confirm the target gene of miR-338-3p in cervical cancer cells.

Results: In the present work, our data showed that the expression of miR-338-3p was substantially decreased in cervical cancer tissues and associated with advanced FIGO stage, lymph node metastasis, depth of cervical invasion and poor overall survival. However, the MACC1 had an opposite expression. Mechanistically, we identified that MACC1 which acted as a functional downstream target for miR-338-3p. Furthermore, overexpression of miR-338-3p decreased expression of MACC1 in cervical cancer cells could significantly inhibit cervical cancer cell proliferation and induce cells apoptosis. Interestingly, miR-338-3p and MACC1 had proven to be involved in the progression of cervical cancer cells by regulating mitogen-activated protein kinase (MAPK) signaling pathway.

Conclusions: Our results suggested miR-338-3p/MACC1/MAPK regulatory pathway play an important role in the progression of cervical cancer.

MeSH terms

  • Adult
  • Aged
  • Cell Line, Tumor
  • Cell Proliferation / genetics
  • Female
  • Humans
  • MAP Kinase Signaling System / physiology*
  • MicroRNAs / physiology*
  • Middle Aged
  • Trans-Activators
  • Transcription Factors / genetics
  • Transcription Factors / physiology*
  • Uterine Cervical Neoplasms / etiology
  • Uterine Cervical Neoplasms / genetics
  • Uterine Cervical Neoplasms / pathology*


  • MACC1 protein, human
  • MIRN338 microRNA, human
  • MicroRNAs
  • Trans-Activators
  • Transcription Factors