Screening for breast cancer.

EMT mechanism in breast cancer metastasis and drug resistance: Revisiting molecular interactions and biological functions.

Breast cancer (BC) remains the most frequently diagnosed cancer worldwide. Among breast cancer patients, distant metastasis and invasion is the leading cause of BC related death. Recently, long non-coding RNAs (lncRNAs), which used to be considered a genetic byproduct (owing to their unknown biological function), have been reported to be highly implicated in the development and progression of BC. In this review, we produce a summary of the functions and mechanisms of lncRNAs implicated in the different distant metastases of BC. The functions of lncRNAs have been divided into two types: oncogenic type and tumor suppressor. Furthermore, the majority of them exert their roles through the regulation of invasion, migration, epithelial-mesenchymal transition (EMT), and the metastasis process. In the final part, we briefly addressed future research prospects of lncRNAs, especially the testing methods through which to detect lncRNAs in the clinical work, and introduced several different tools with which to detect lncRNAs more conveniently. Although lncRNA research is still in the initial stages, it is a promising prognosticator and a novel therapeutic target for BC metastasis, which requires more research in the future.

/pdf/the-role-of-lncrnas-in-the-distant-metastasis-of-breast-4y1zpi9zg4.pdf

The Role of lncRNAs in the Distant Metastasis of Breast Cancer

Long non-coding RNAs and cancer metastasis: Molecular basis and therapeutic implications.

Dissecting miRNA signature in colorectal cancer progression and metastasis.

Breast cancer was dangerous to women health. A growing number of evidences indicate that long non-coding RNAs (lncRNAs) have many functions in the development and progression of breast cancer and may serve as the markers of diagnosis or prognosis. BLACAT1 is one of lncRNA and the roles of it in breast cancer is not clear. In this study, it is aimed to explore the roles and molecular mechanisms of BLACAT1 in breast cancer. We found BLACAT1 took part in breast cancer cell aggressive phenotype. The real-time PCR result showed that BLACAT1 was up-regulated in tumor tissues compared to adjacent normal tissues. The molecular mechanism experiments demonstrated that BLACAT1 down-regulation suppressed the proliferation and metastasis of human breast cancer cells by regulating miR-150-5p targeting CCR2. The clinical studies indicated that lack of BLACAT1 was related to tumor size, metastasis. Conclusion: The present study verified the involvement of the BLACAT1 in the mediation of cell survival and metastasis through miR-150-5p targeting CCR2 in breast cancer cells.

/pdf/long-non-coding-rna-blacat1-promotes-breast-cancer-cell-4nt61sy9ao.pdf

Long non-coding RNA BLACAT1 promotes breast cancer cell proliferation and metastasis by miR-150-5p/CCR2

Breast cancer (BC) represents the most commonly diagnosed malignancy among women. Long non-coding RNAs (lncRNAs) can be transferred by extracellular vesicles (EVs) to participate in BC progression. This study demonstrated that SNHG16 expression was significantly increased in BC tissues and cells. Overexpression of SNHG16 promoted the migration, invasion, and epithelial-mesenchymal transition (EMT) of BC cells. SNHG16 was carried by EVs. Bioinformatics analysis predicted that SNHG16 regulated PPAPDC1A expression by sponging miR-892b, which was confirmed by RNA-fluorescence in situ hybridization (FISH), RT-qPCR, dual-luciferase gene reporter assay, and RNA immunoprecipitation (RIP). MDA-MB-157 and HS578T cells were transfected with pcDNA3.1-SNHG16, miR-892b-mimic, or si-PPAPDC1A for functional rescue experiments in vitro, and the cells were treated with MDA-MB-231 cell-derived EVs. The results confirmed that enhanced miR-892b expression partially eliminated the increase of migration, invasion, and EMT of BC cells mediated by SNHG16 or EVs. The lung metastasis model in nude mice was established by injecting HS578T cells via tail vein. The results showed that si-SNHG16 reduced the metastatic nodules and decreased the vimentin expression. In conclusion, EVs derived from BC cells transferred SNHG16 via the miR-892b/PPAPDC1A axis, thus promoting EMT, migration, and invasion of BC.

/pdf/extracellular-vesicles-carry-lncrna-snhg16-to-promote-416liplir3.pdf

Extracellular Vesicles Carry lncRNA SNHG16 to Promote Metastasis of Breast Cancer Cells via the miR-892b/PPAPDC1A Axis.

Assembling evidences suggested that aberrant expression of tissue differentiation-inducing non-protein coding RNA (TINCR) intimately associated with variety of human cancer. However, the expression pattern and involvement of TINCR in breast cancer has not been fully investigated. Here we set out to analyze expression of TINCR in breast cancer and elucidate its mechanistic involvement in tumor incidence and progression. The expression of TINCR was determined by q-PCR. SP1 binding sites were analyzed by ChIP-qPCR. The relative transcription activity was measured with luciferase reporter assay. Cell viability was measured with CCK-8 method. Clonogenic capacity was evaluated by soft agar assay. Cell apoptosis was analyzed by Annexin V/7-AAD staining. The migration and invasion were determined by trans-well assay and wound healing. The tumor growth in vivo was evaluated in xenograft mice model. Protein expression was quantified by immunoblotting. TINCR was aberrantly up-regulated by SP1, which in turn stimulated cell proliferation, anchorage-independent growth and suppressed cell apoptosis in breast cancer. TINCR silencing significantly suppressed migration and invasion in vitro and xenograft tumor growth in vivo. Mechanistically, TINCR modulated KLF4 expression via competing with miR-7, which consequently contributed to its oncogenic potential. MiR-7 inhibition severely compromised TINCR silencing-elicited tumor repressive effects. Our data uncovered a crucial role of TINCR-miR-7-KLF4 axis in human breast cancer.

/pdf/up-regulation-of-cerna-tincr-by-sp1-contributes-to-2hz982igwy.pdf

Up-regulation of ceRNA TINCR by SP1 contributes to tumorigenesis in breast cancer.

Long non-coding RNAs (lncRNAs) are novel regulatory molecules in breast cancer development. LncRNA LUCAT1 is a potential tumor promoter in human cancers. In this study, we aimed to explore the role of LUCAT1 in human breast cancer tissues and cells. A total of 31 breast cancer patients who underwent tumor resection, but without chemo- or radiotherapy or acute lung/heart/kidney diseases, provided tumor and adjacent normal tissues. Bioinformatic analysis, qRT-PCR, and luciferase reporter assay were carried out during the study. qRT-PCR analysis indicated that, compared with the adjacent tissues and MCF-10A normal breast epithelial cells, LUCAT1 was markedly up-regulated in the breast cancer tissues and five BC cell lines, including MDA-MB-231, MDA-MB-468, MDA-MB-435, SKBR3, and MCF-7. The knockdown of LUCAT1, through the transfection of small interfering RNA (siRNA) specific to LUCAT1, resulted in inhibition of proliferation in breast cancer cells. The expression levels of miR-181a-5p were decreased in the breast cancer tissues and five BC cell lines. Bioinformatic analysis and luciferase reporter assay suggested the interaction between miR-181a-5p and LUCAT1. In addition, the effects of LUCAT1 on promoting cell proliferation were attenuated by overexpression of miR-181a-5p through the transfection of miR-181a-5p mimic. Moreover, bioinformatics and luciferase reporter assay confirmed that miR-181a-5p targeted the 3′-UTR region of KLF6 and KLF15 mRNA, which were two tumor suppressor genes. LUCAT1/miR-181a-5p axis regulated the expression of KLF6 and KLF15 both in vitro and in vivo. Our data indicate that LUCAT1/miR-181a-5p axis can serve as a novel therapeutic target in breast cancer.

/pdf/lncrna-lucat1-mir-181a-5p-axis-promotes-proliferation-and-4dyd8ujpjy.pdf

LncRNA LUCAT1/miR-181a-5p axis promotes proliferation and invasion of breast cancer via targeting KLF6 and KLF15

Background/aims The effects of microRNA-423 on proliferation and drug resistance of breast cancer cells were explored, the downstream target genes of miR-423 and the targeted regulatory relationship between them were studied. Methods RT-qPCR was used to detect the expression of miR-423 in breast cancer tissues and cell lines, and the transfection efficiency of miR-423 inhibitory vector miR-423-inhibitor was constructed and verified. CCK-8 and colony formation assays were used to examine the effect of miR-423 on tumor cell proliferation. Target gene prediction and screening and luciferase reporter assay were used to verify downstream target genes of miR-432. The mRNA and protein expression of miR-423target gene ZFP36 was detected by RT-qPCR and Western blotting. Results The expression of miR-423 was significantly higher than that in normal tissues. Compared to the non-malignant mammary epithelial cell line MCF-10A, the expression of miR-423 was significantly raised in MCR-7 and MCF-7/ADR cells. ZFP36 was a downstream target gene of miR-423 and negatively correlated with the expression of miR-423 in breast cancer. The knockdown of miR-423 can significantly enhance the cytotoxicity of the drug, increase the apoptotic rate of MCF-7/ADR cells. miR-423 was capable of activating the Wnt/β-catenin signaling pathway leading to chemoresistance and proliferation, whereas overexpression of ZFP36 reduced drug resistance and proliferation. Conclusion miR-423 acted as an oncogene to promote tumor cell proliferation and migration. ZFP36 was a downstream target gene of miR-423, and miR-423 inhibited the expression of ZFP36 via Wnt/β-catenin signaling pathway of breast cancer cells.

/pdf/microrna-423-drug-resistance-and-proliferation-of-breast-1b4110agn7.pdf

MicroRNA-423 Drug Resistance and Proliferation of Breast Cancer Cells by Targeting ZFP36.

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