The emerging role of miR‐375 in cancer

Yan, Junwei; Lin, Ju‐Sheng; He, Xingxing

doi:10.1002/ijc.28563

Cited by 215 publications

(192 citation statements)

References 98 publications

(207 reference statements)

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“…Finally, the underlying cell intrinsic mechanism for PDPK1 activation in myeloma cells remains to be verified in this study. Recent studies have indicated that the deregulation of miRNA-375 (miR375) associates with the deregulated expression and activity of PDPK1 in various cancers (49). Moreover, our preliminary data coincide with the previous finding that reported the decreased expression of miR375 in a large majority of patients with multiple myeloma regardless of their cytogenetic features (50).…”

Section: Discussionsupporting

confidence: 90%

Phosphoinositide Protein Kinase PDPK1 Is a Crucial Cell Signaling Mediator in Multiple Myeloma

et al. 2014

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Multiple myeloma is a cytogenetically/molecularly heterogeneous hematologic malignancy that remains mostly incurable, and the identification of a universal and relevant therapeutic target molecule is essential for the further development of therapeutic strategy. Herein, we identified that 3-phosphoinositide-dependent protein kinase 1 (PDPK1), a serine threonine kinase, is expressed and active in all eleven multiple myeloma-derived cell lines examined regardless of the type of cytogenetic abnormality, the mutation state of RAS and FGFR3 genes, or the activation state of ERK and AKT. Our results revealed that PDPK1 is a pivotal regulator of molecules that are essential for myelomagenesis, such as RSK2, AKT, c-MYC, IRF4, or cyclin Ds, and that PDPK1 inhibition caused the growth inhibition and the induction of apoptosis with the activation of BIM and BAD, and augmented the in vitro cytotoxic effects of antimyeloma agents in myeloma cells. In the clinical setting, PDPK1 was active in myeloma cells of approximately 90% of symptomatic patients at diagnosis, and the smaller population of patients with multiple myeloma exhibiting myeloma cells without active PDPK1 showed a significantly less frequent proportion of the disease stage III by the International Staging System and a significantly more favorable prognosis, including the longer overall survival period and the longer progression-free survival period by bortezomib treatment, than patients with active PDPK1, suggesting that PDPK1 activation accelerates the disease progression and the resistance to treatment in multiple myeloma. Our study demonstrates that PDPK1 is a potent and a universally targetable signaling mediator in multiple myeloma regardless of the types of cytogenetic/molecular profiles. Cancer Res; 74(24); 7418-29. Ó2014 AACR.

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Section: Discussionsupporting

confidence: 90%

Phosphoinositide Protein Kinase PDPK1 Is a Crucial Cell Signaling Mediator in Multiple Myeloma

et al. 2014

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“…This approach has led to the identification of EYA2 and hsa-mir-375 as novel onco-and tumour suppressor genes, respectively, in cervical cancer 43 . In support of these findings, EYA2 has recently been identified as a target of viral integration and a tumour suppressive function of miR-375 has also been corroborated in other studies 44,45 . These data provide a proof-of-concept that specific chromosomal aberrations can contribute to HPV-induced carcinogenesis.…”

Section: Chromosomal Aberrationssupporting

confidence: 72%

“…According to their epidemiological association with cervical cancer and consolidated by biological studies, twelve HPV types (HPV 16,18,31,33,35,39,45, 51, 52, 56, 58 and 59) have now been consistently classified as hrHPV (also known as IARC class I). HPV 68 has been classified as probable high-risk (also known as IARC class 2A) and another seven types have been classified as possible high-risk (HPV 26,53,66,67,70,73 and 82;also known as IARC class 2B) 5 .…”

Section: Cervical Cancer and Hpvmentioning

confidence: 99%

Clinical implications of (epi)genetic changes in HPV-induced cervical precancerous lesions

et al. 2014

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PrefaceInfection of cervical epithelium with high-risk human papillomavirus (hrHPV) might result in productive or transforming cervical intraepithelial neoplasia (CIN) lesions, the morphology of which can overlap. In transforming CIN lesions aberrations in host cell genes accumulate over time, which is necessary for ultimate progression to cancer. On the basis of (epi)genetic changes, early and advanced transforming CIN lesions can be distinguished. This paves the way for new molecular tools for cervical screening, diagnosis and management of cervical cancer precursor lesions.

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“…Finally, a recent review by Yan et al emphasized the emerging role of miR-375 in cancer and specified that miR-375 is frequently downregulated in multiple types of cancer, especially in hepatocarcinoma, 42 esophagus cancer, 43 osteosarcoma, 44 lung cancer, 45 and acts as a tumor suppressor by repressing many critical oncogenes such as PDK1, JAK2, IGF1R, 46 AEG-1, 42 and suppressing the PI3K/Akt pathway. 44 Furthermore, miR-375 might be used as a diagnostic and prognostic biomarker in various cancers.…”

Section: Discussionmentioning

confidence: 99%

Identification of microRNA expression profile related to lymph node status in women with early-stage grade 1–2 endometrial cancer

et al. 2016

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Conventional methods used for histologic classification and grading of endometrial cancer (EC) are not sufficient to predict lymph node metastases. microRNA signatures have recently been related to EC pathologic characteristics or prognosis. The aim of this study was to evaluate whether microRNA profiles of grade 1-2 endometrioid adenocarcinomas can be related to nodal status and used as a tool to adapt surgical staging in early-stage EC. microRNA expression was assessed in nine formalin-fixed paraffin-embedded (FFPE) EC primary tumors with positive lymph node and in 27 FFPE EC primary tumors with negative lymph node, matched for grade, stage, and lymphovascular space involvement status. A microarray analysis showed that there was more than a twofold significant difference in the expression of 12 microRNAs between the two groups. A quantitative reverse transcriptase-PCR assay was used to confirm these results: the expression levels of five microRNAs (microRNA-34c-5p, -375, -184, -34c-3p, and -34b-5p) were significantly lower in the EC primary tumor with positive lymph node compared with those with negative lymph node. A minimal P-value approach revealed that women with a microRNA-375-fold change o 0.30 were more likely to have positive lymph node (n = 8; 53.3%) compared with those with a microRNA-375-fold change 40.30 (n = 1; 4.8%), P = 0.001. Furthermore, women with a microRNA 184-fold change o0.30 were more likely to have positive lymph node (n = 6; 60.0%) compared with those with a microRNA 184-fold change 40.30 (n = 3; 11.5%), P = 0.006. This is the first study investigating the relative expression of mature microRNA genes in early-stage grade 1-2 EC primary tumors according to the nodal status. This microRNA expression profile provides a potential basis for further study of the microRNA function in EC and could be used as a diagnostic tool for nodal status.

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The emerging role of miR‐375 in cancer

Cited by 215 publications

References 98 publications

Phosphoinositide Protein Kinase PDPK1 Is a Crucial Cell Signaling Mediator in Multiple Myeloma

Phosphoinositide Protein Kinase PDPK1 Is a Crucial Cell Signaling Mediator in Multiple Myeloma

Clinical implications of (epi)genetic changes in HPV-induced cervical precancerous lesions

Identification of microRNA expression profile related to lymph node status in women with early-stage grade 1–2 endometrial cancer

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