Reprimo as a modulator of cell migration and invasion in the MDA-MB-231 breast cancer cell line

Buchegger, Kurt; Ili, Carmen; Riquelme, Ismael; Letelier, Pablo; Corvalán, Alejandro; Brebi-Mieville, Priscilla; Huang, Tim H.M.; Roa, Juan Carlos

doi:10.1186/s40659-016-0066-7

Cited by 15 publications

(15 citation statements)

References 30 publications

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“…In this study, we show for the first time that the CHL1 gene, located in this region, is silenced in a subset of invasive BC cases due to promoter hypermethylation, but not in adjacent-to-tumour tissue and non-neoplastic tissue from mammoplasties. This epigenetic alteration has been found by pyrosequencing, a technique that yields quantitative measurements of methylation in contrast to methylation-specific PCR [29–33]. Consistent with the observed hypermethylation, we have found that tumour cells in BC tissues have a lower level of CHL1 expression compared with non-neoplastic adjacent-to-tumour cells.…”

Section: Discussionsupporting

confidence: 88%

CHL1 hypermethylation as a potential biomarker of poor prognosis in breast cancer

et al. 2017

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The CHL1 gene encodes a cell-adhesion molecule proposed as being a putative tumour-suppressor gene in breast cancer (BC). However, neither the underlying molecular mechanisms nor the clinical value of CHL1 downregulation in BC has been explored. The methylation status of three CpG sites in the CHL1 promoter was analysed by pyrosequencing in neoplastic biopsies from 142 patients with invasive BC and compared with that of non-neoplastic tissues. We found higher CHL1 methylation levels in breast tumours than in non-neoplastic tissues, either from mammoplasties or adjacent-to-tumour, which correlated with lower levels of protein expression in tumours measured by immunohistochemistry. A panel of five BC cell lines was treated with two epigenetic drugs, and restoration of CHL1 expression was observed, indicating in vitro dynamic epigenetic regulation. CHL1 was silenced by shRNA in immortalized but non-neoplastic mammary cells, and enhanced cell proliferation and migration, but not invasion, were found by real-time cell analysis. The prognostic value of CHL1 hypermethylation was assessed by the log-rank test and fitted in a Cox regression model. Importantly, CHL1 hypermethylation was very significantly associated with shorter progression-free survival in our BC patient series, independent of age and stage (p = 0.001). In conclusion, our results indicate that CHL1 is downregulated by hypermethylation and that this epigenetic alteration is an independent prognostic factor in BC.

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Section: Discussionsupporting

confidence: 88%

CHL1 hypermethylation as a potential biomarker of poor prognosis in breast cancer

et al. 2017

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“…Interesting results were proposed by Buchegger et al [ 85 ]. They suggested potential mechanism of migration of MDA-MB-231 cells.…”

Section: Discussionmentioning

confidence: 98%

Migration Rate Inhibition of Breast Cancer Cells Treated by Caffeic Acid and Caffeic Acid Phenethyl Ester: An In Vitro Comparison Study

et al. 2017

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One of the deadliest cancers among women is a breast cancer. Research has shown that two natural substances occurring in propolis, caffeic acid (CA) and caffeic acid phenethyl ester (CAPE), have significant anticancer effects. The purpose of our in vitro study was to compare cytotoxic activity and migration rate inhibition using CA and CAPE (doses of 50 and 100 µm) against triple-negative, MDA-MB-231 breast adenocarcinoma line cells, drawn from Caucasian women. Viability was measured by XTT-NR-SRB assay (Tetrazolium hydroxide-Neutral Red-Sulforhodamine B) for 24 h and 48 h periods. Cell migration for wound healing assay was taken for 0 h, 8 h, 16 h, and 24 h periods. CAPE displayed more than two times higher cytotoxicity against MDA-MB-231 cells. IC50 values for the XTT assay were as follows: CA for 24 h and 48 h were 150.94 µM and 108.42 µM, respectively, while CAPE was 68.82 µM for 24 h and 55.79 µM for 48 h. For the NR assay: CA was 135.85 µM at 24 h and 103.23 µM at 48 h, while CAPE was 64.04 µM at 24 h and 53.25 µM at 48 h. For the SRB assay: CA at 24 h was 139.80 µM and at 48 h 103.98 µM, while CAPE was 66.86 µM at 24 h and 47.73 µM at 48 h. Both agents suspended the migration rate; however, CAPE displayed better activity. Notably, for the 100 µM CAPE dose, motility of the tested breast carcinoma cells was halted.

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“…Correspondingly, mouse xenografts models of gastric cancer cells deficient in RPRM expression have demonstrated enhanced tumor formation and volume [ 31 , 32 ]. In other tumors, such as breast cancer, pituitary tumors and renal cell carcinoma cell lines, overexpression of RPRM suppresses cell proliferation, cell migration, clonogenic capacity and invasiveness [ 33 , 34 , 35 ]. Furthermore, the role of RPRM in cell-cycle has also been explored.…”

Section: Role Of the Rprm Gene Family In Human mentioning

confidence: 99%

The Reprimo Gene Family: A Novel Gene Lineage in Gastric Cancer with Tumor Suppressive Properties

Amigo

Opazo

Jorquera

et al. 2018

IJMS

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The reprimo (RPRM) gene family is a group of single exon genes present exclusively within the vertebrate lineage. Two out of three members of this family are present in humans: RPRM and RPRM-Like (RPRML). RPRM induces cell cycle arrest at G2/M in response to p53 expression. Loss-of-expression of RPRM is related to increased cell proliferation and growth in gastric cancer. This evidence suggests that RPRM has tumor suppressive properties. However, the molecular mechanisms and signaling partners by which RPRM exerts its functions remain unknown. Moreover, scarce studies have attempted to characterize RPRML, and its functionality is unclear. Herein, we highlight the role of the RPRM gene family in gastric carcinogenesis, as well as its potential applications in clinical settings. In addition, we summarize the current knowledge on the phylogeny and expression patterns of this family of genes in embryonic zebrafish and adult humans. Strikingly, in both species, RPRM is expressed primarily in the digestive tract, blood vessels and central nervous system, supporting the use of zebrafish for further functional characterization of RPRM. Finally, drawing on embryonic and adult expression patterns, we address the potential relevance of RPRM and RPRML in cancer. Active investigation or analytical research in the coming years should contribute to novel translational applications of this poorly understood gene family as potential biomarkers and development of novel cancer therapies.

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Reprimo as a modulator of cell migration and invasion in the MDA-MB-231 breast cancer cell line

Cited by 15 publications

References 30 publications

CHL1 hypermethylation as a potential biomarker of poor prognosis in breast cancer

CHL1 hypermethylation as a potential biomarker of poor prognosis in breast cancer

Migration Rate Inhibition of Breast Cancer Cells Treated by Caffeic Acid and Caffeic Acid Phenethyl Ester: An In Vitro Comparison Study

The Reprimo Gene Family: A Novel Gene Lineage in Gastric Cancer with Tumor Suppressive Properties

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