LncRNAs as new biomarkers to differentiate triple negative breast cancer from non-triple negative breast cancer

Lv, Mingming; Xu, Pengfei; Wu, Ying; Huang, Lei; Li, Wenqu; Lv, Shanshan; Wu, Xiaowei; Zeng, Xin; Shen, Rong; Jia, Xuemei; Yin, Yongmei; Gu, Yun; Yuan, Hongyan; Xie, Hui; Fu, Ziyi

doi:10.18632/oncotarget.7509

Cited by 83 publications

(85 citation statements)

References 52 publications

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“…U6 were used as an internal control [21,40]. The 2 −ΔΔCt and ΔCt [34,41] methods were used for analysis of the differential expression of tRFs in cells and serum samples, respectively. The names of tRFs, their sequences and specific primer sequence are given in Supplementary Table 2.…”

Section: Quantitative Real-time Pcrmentioning

confidence: 99%

tRNA-Derived Fragments as Novel Predictive Biomarkers for Trastuzumab-Resistant Breast Cancer

Sun

Yang

Zhang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Resistance to trastuzumab remains a common challenge to HER-2 positive breast cancer. Up until now, the underlying mechanism of trastuzumab resistance is still unclear. tRNA-derived small non-coding RNAs, a new class of small non-coding RNA (sncRNAs), have been observed to play an important role in cancer progression. However, the relationship between tRNA-derived fragments and trastuzumab resistance is still unknown. Methods: We detected the levels of tRNA-derived fragments expression in normal breast epithelial cell lines, trastuzumab-sensitive and -resistant breast cancer cell lines using high-throughput sequencing. qRT-PCR was conducted to validate the differentially expressed fragments in serums from trastuzumab-sensitive and -resistant patients. A receiver operating characteristic (ROC) curve analysis was performed to evaluate the power of specific tRNA-derived fragments. Progression-free survival (PFS) was analyzed using Cox-regression. Results: Our sequence results showed that tRNA-derived fragments were differentially expressed in the HBL-100, SKBR3, and JIMT-1 cell lines. tRF-30-JZOYJE22RR33 and tRF-27-ZDXPHO53KSN were found significantly upregulated in trastuzumab-resistant patients compared to sensitive individuals, and the ROC analysis showed that tRF-30-JZOYJE22RR33 and tRF-27-ZDXPHO53KSN were correlated with trastuzumab resistance. In a multivariate analysis, higher levels of tRF-30-JZOYJE22RR33 and tRF-27-ZDXPHO53KSN expression were associated with significantly shorter PFS in patients with metastatic HER-2 positive breast cancer. Conclusion: Our results suggest that tRF-30-JZOYJE22RR33 and tRF-27-ZDXPHO53KSN play important roles in trastuzumab resistance. Patients with high levels of tRF-30-JZOYJE22RR33 and tRF-27-ZDXPHO53KSN expression benefitted less from trastuzumab-based therapy than those that express lower-levels of these molecules. tRF-30-JZOYJE22RR33 and tRF-27-ZDXPHO53KSN may be potential biomarkers and intervention targets in the clinical treatment of trastuzumab-resistant breast cancer.

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Section: Quantitative Real-time Pcrmentioning

confidence: 99%

tRNA-Derived Fragments as Novel Predictive Biomarkers for Trastuzumab-Resistant Breast Cancer

Sun

Yang

Zhang

et al. 2018

Cell Physiol Biochem

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“…Moreover, it could bind to miR‐452‐5p as a sponge and downregulated its target gene, erythrocyte membrane protein band 4.1 like 3 (EPB41L3), in HCC . In addition to its effects in HCC, researchers found that LINC00052 had a significant effect on gastric cancer and breast cancer . Despite these findings, LINC00052's function in CRC has not been studied.…”

Section: Introductionmentioning

confidence: 99%

Retracted: Long noncoding RNA LINC00052 inhibits colorectal cancer metastasis by sponging microRNA‐574‐5p to modulate CALCOCO1 expression

Xiong

Liu

et al. 2019

J of Cellular Biochemistry

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The dysregulation of long‐chain noncoding ribonucleic acid (lncRNA) is a common phenomenon in many human cancers. Some studies on the biological function of long intergenic non‐protein‐coding RNA 52 (LINC00052) in cancer indicate that this gene can act as either oncogene or tumor suppressor in some kinds of cancers, such as breast cancer, gastric cancer, liver cancer, and lung cancer. However, the biological function of LINC00052 in colorectal cancer (CRC) has not been studied. Quantitative reverse‐transcription polymerase chain reaction (qRT‐PCR) and Western blot (WB) techniques were applied to detect the expression levels of LINC00052, miR‐574‐5p, and calcium‐binding and coiled‐coil domain 1 (CALCOCO1) in CRC cells and tissues. We authenticated the biological function of LINC00052 and miR‐574‐5p in CRC, and find some target genes for LINC00052 and miR‐574‐5p via bioinformatics methods. Dual‐luciferase reporter gene assay was performed to identify the interaction between LINC00052 and miR‐574‐5p or CALCOCO1 and miR‐574‐5p. The results demonstrated that LINC00052 was downregulated in CRC tissues compared with their adjacent tissues. And LINC00052 could suppress CRC cells metastasis both in vivo and in vitro. Beyond that, miR‐574‐5p was upregulated in CRC tissues, and as an oncogene, it accelerated CRC cell migration and invasion. More importantly, the results of our research demonstrated that LINC00052 could regulate the expression of CALCOCO1 via sponging miR‐574‐5p in CRC. Overall, our study illuminated the lncRNA‐miRNA functional networks in CRC, and these results might provide a new research direction for the diagnosis and treatment of CRC.

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“…GO function and KEGG enrichment for differentially expressed genes were used to identify the significantly enriched biological terms and pathways [24]. The database for annotation, visualization, and integrated discover (DAVID) was applied to perform GO function enrichment for differentially expressed genes.…”

Section: Methodsmentioning

confidence: 99%

Benzotriazole Enhances Cell Invasive Potency in Endometrial Carcinoma Through CTBP1-Mediated Epithelial-Mesenchymal Transition

Wang

Dai

Zhou

et al. 2017

Cell Physiol Biochem

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Background/Aims: Benzotriazole (BTR) and its derivatives, such as intermediates and UV stabilizers, are important man-made organic chemicals found in everyday life that have been recently identified as environmental toxins and a threat to female reproductive health. Previous studies have shown that BTR could act as a carcinogen by mimicking estrogen. Environmental estrogen mimics could promote the initiation and development of female cancers, such as endometrial carcinoma, a type of estrogenic-sensitive malignancy. However, there is little information on the relationship between BTR and endometrial carcinoma. In this study, we aimed to demonstrate the biological function of BTR in endometrial carcinoma and explored the underlying mechanism. Methods: The CCK-8 assay was performed to detect cell viability; transwell-filter assay was used to assess cell invasion; gene microarray analysis was employed to determine gene expression patterns in response to BTR treatment; western blotting and quantitative reverse transcription polymerase chain reaction (qRT-PCR) were carried out to detect the expression levels of BTR-related genes. Results: Our data showed that BTR could induce the invasion and migration of endometrial carcinoma cells (Ishikawa and HEC-1-B). In addition, BTR increased the expression level of CTBP1, which could enhance the epithelial-mesenchymal transition (EMT) in cancer cells. Moreover, CTBP1 silencing reversed the effect of BTR on EMT progression in endometrial carcinoma cells. Conclusion: This study indicates that BTR could act as a carcinogen to promote the development of endometrial carcinoma mainly through CTBP1-mediated EMT, which deserves more attention.

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LncRNAs as new biomarkers to differentiate triple negative breast cancer from non-triple negative breast cancer

Cited by 83 publications

References 52 publications

tRNA-Derived Fragments as Novel Predictive Biomarkers for Trastuzumab-Resistant Breast Cancer

tRNA-Derived Fragments as Novel Predictive Biomarkers for Trastuzumab-Resistant Breast Cancer

Retracted: Long noncoding RNA LINC00052 inhibits colorectal cancer metastasis by sponging microRNA‐574‐5p to modulate CALCOCO1 expression

Benzotriazole Enhances Cell Invasive Potency in Endometrial Carcinoma Through CTBP1-Mediated Epithelial-Mesenchymal Transition

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