Circular RNA circABCC4 acts as a ceRNA of miR-154-5p to improve cell viability, migration and invasion of breast cancer cells in vitro

Abstract Background Opioid receptors are implicated in cell proliferation and cancer migration. However, the effects and underlying mechanisms of opioid receptor κ (OPRK1) in breast cancer remain unknown. Methods Small interfering RNA (siRNAs) was used to knockdown the expression of OPRK1. Western blot was used to determine the protein expression and reverse transcription-quantitative PCR (RT-qPCR) determined the genes transcription. Cell viability was detected by MTT assay and cell death rates were determined by Annexin V/PI and flow cytometry. Cell migration and invasion were detected by wound healing analysis and transwell assay, respectively. Results Our research demonstrated that OPRK1 was overexpressed in breast cancer cells compared with the normal human mammary epithelial cells. OPRK1 knockdown could inhibited cell viability and migration in cancer cells, accompanied with the decreased proteins and genes expression of N-cadherin, Snail, MMP2 and Vimentin, while the E-cadherin expression was increased. Additionally, OPRK1 knockdown also promoted PI3K/AKT signaling inactivation. Activation of AKT reversed the OPRK1 knockdown-induced cell viability inhibition and migration suppression, while inhibition of AKT reduced cell viability and promoted cell death. Conclusions Our findings illustrated the role of OPRK1 played on promoting migration in vitro, and we also provided the therapeutic research of OPRK1 knockdown combined with AKT inhibition.

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Circular RNA circ-MMP11 Contributes to Lapatinib Resistance of Breast Cancer Cells by Regulating the miR-153-3p/ANLN Axis

Frontiers in Oncology ◽

10.3389/fonc.2021.639961 ◽

2021 ◽

Vol 11 ◽

Author(s):

Xiaoli Wu ◽

Yi Ren ◽

Rong Yao ◽

Leilei Zhou ◽

Ruihua Fan

Keyword(s):

Breast Cancer ◽

Drug Resistance ◽

Cell Viability ◽

Cancer Cells ◽

Breast Cancer Cells ◽

Quantitative Polymerase Chain Reaction ◽

Circular Rna ◽

Luciferase Reporter ◽

Migration And Invasion

BackgroundDrug-resistance is a major obstacle to the treatment of breast cancer. Circular RNA (circRNA) circ-MMP11 has been reported to be promoting the progression of breast cancer. This study is designed to explore the role and mechanism of circ-MMP11 in lapatinib resistance in breast cancer.MethodsCirc-MMP11, microRNA-153-3p (miR-153-3p), and Anillin (ANLN) levels were detected by real-time quantitative polymerase chain reaction (RT-qPCR). Cell viability, number of colonies, apoptosis, migration, and invasion were detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT), colony formation, flow cytometry, and transwell assays, respectively. Exosomes were exerted and detected by differential centrifugation and a transmission electron microscope. The protein levels of CD63, CD9, and ANLN were assessed by western blot assay. The binding relationship between miR-153-3p and circ-MMP11 or ANLN was predicted by circinteractome or starbase, and then verified by a dual-luciferase reporter assay and RNA pull-down assay. The biological role of circ-MMP11 on breast cancer tumor growth and drug resistance was detected by the xenograft tumor model in vivo.ResultsCirc-MMP11 and ANLN were highly expressed, and miR-153-3p was decreased in LR breast cancer tissues and cells. Circ-MMP11 could be transported by exosomes. Furthermore, circ-MMP11 knockdown promoted lapatinib sensitivity by repressing cell viability, colony number, migration, invasion, and boosting apoptosis in LR breast cancer cells. Circ-MMP11 deficiency improved the drug sensitivity of breast cancer in vivo. Mechanically, circ-MMP11 could regulate ANLN expression through sponging miR-153-3p.ConclusionCirc-MMP11 could be transferred by exosomes in breast cancer cells. And circ-MMP11 functioned as a sponge of miR-153-3p to regulate ANLN expression, thereby promoting lapatinib resistance in breast cancer cells, providing therapeutic targets for the treatment of breast cancer.

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In vivo and in vitro effects of microRNA-27a on proliferation, migration and invasion of breast cancer cells through targeting of SFRP1 gene via Wnt/β-catenin signaling pathway

Oncotarget ◽

10.18632/oncotarget.14662 ◽

2017 ◽

Vol 8 (9) ◽

pp. 15507-15519 ◽

Cited By ~ 36

Author(s):

Ling-Yu Kong ◽

Mei Xue ◽

Qing-Cai Zhang ◽

Chuan-Fu Su

Keyword(s):

Breast Cancer ◽

Cancer Cells ◽

Signaling Pathway ◽

Breast Cancer Cells ◽

Migration And Invasion ◽

In Vitro Effects

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The long noncoding RNA AATBC promotes breast cancer migration and invasion by interacting with YBX1 and activating the YAP1/Hippo signaling pathway

10.21203/rs.3.rs-141063/v1 ◽

2021 ◽

Author(s):

Maonan Wang ◽

Manli Dai ◽

Dan Wang ◽

Ting Tang ◽

Fang Xiong ◽

...

Keyword(s):

Breast Cancer ◽

Cancer Cells ◽

Signaling Pathway ◽

Breast Cancer Cells ◽

Differentially Expressed ◽

Migration And Invasion ◽

Hippo Signaling ◽

Hippo Signaling Pathway

Abstract BackgroundLong noncoding RNAs (lncRNAs) play an important role in the regulation of gene expression and are involved in several pathological responses. However, many important lncRNAs in breast cancer have not been identified and their expression levels and functions in breast cancer remain unknown.MethodsWe used the microarray data to identify differentially expressed lncRNAs between breast cancer and adjacent breast epithelial tissues. In vitro and in vivo assays were used to explore the biological effects of the differentially expressed lncRNA Apoptosis-Associated Transcript in Bladder Cancer (AATBC) in breast cancer cells. The mass spectrometry and RNA pulldown were used to screen AATBC interacting proteins. Using the Kaplan-Meier method, survival analysis was performed.ResultsThe expression of AATBC was significantly high in breast cancer samples, and this high AATBC level was tightly correlated with poor prognosis in breast cancer patients. In vitro and in vivo experiments indicated that AATBC promoted breast cancer cells migration and invasion. AATBC specifically interacted with Y-box binding protein 1 (YBX1), which activated the YAP1/Hippo signaling pathway by binding to macrophage stimulating 1 (MST1) and promoting the nuclear translocation of Yes associated protein 1 (YAP1), allowing its function as a nuclear transcriptional regulator. ConclusionsAATBC is highly expressed in breast cancer and contributes to patients’ progression, indicating that it could serve as a novel prognostic marker for the disease. Mechanistically, AATBC affects migration and invasion of breast cancer cells through an AATBC-YBX1-MST1 axis, resulting in activating the YAP1/Hippo signaling pathway. This is also an important supplement to the composition of the YAP1/Hippo signaling pathway. The model of “AATBC-YAP1” may bring a new dawn to the treatment of breast cancer.

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LncRNA LGALS8-AS1 Promotes Breast Cancer Metastasis Through miR-125b-5p/SOX12 Feedback Regulatory Network

Frontiers in Oncology ◽

10.3389/fonc.2021.711684 ◽

2021 ◽

Vol 11 ◽

Author(s):

Duanyang Zhai ◽

Tianfu Li ◽

Runyi Ye ◽

Jiong Bi ◽

Xiaying Kuang ◽

...

Keyword(s):

Breast Cancer ◽

Cancer Cells ◽

Breast Cancer Cells ◽

Cancer Metastasis ◽

Migration And Invasion ◽

Metastatic Progression ◽

Breast Cancer Patients ◽

Term Survival ◽

Regulatory Loop

BackgroundMetastasis is a major factor weakening the long-term survival of breast cancer patients. Increasing evidence revealed that long non-coding RNAs (lncRNAs) were involved in the occurrence and development of breast cancer. In this study, we aimed to investigate the role of LGALS8-AS1 in the metastatic progression of breast cancer cells and its potential mechanisms.ResultsThe lncRNA LGALS8-AS1 was highly expressed in breast cancer and associated with poor survival. LGALS8-AS1 functioned as an oncogenic lncRNA that promoted the metastasis of breast cancer both in vitro and in vivo. It upregulated SOX12 via competing as a competing endogenous RNA (ceRNA) for sponging miR-125b-5p and acted on the PI3K/AKT signaling pathway to promote the metastasis of breast cancer. Furthermore, SOX12, in turn, activated LGALS8-AS1 expression via direct recognition of its sequence binding enrichment motif on the LGALS8-AS1 promoter, thereby forming a positive feedback regulatory loop.ConclusionThis study manifested a novel mechanism of LGALS8-AS1 facilitating the metastasis of breast cancer. The LGALS8-AS1/miR-125b-5p/SOX12 reciprocal regulatory loop dyscrasia promoted the migration and invasion of breast cancer cells. This signaling axis could be applicable to the design of novel therapeutic strategies against this malignancy.

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Crizotinib, a MET inhibitor, inhibits growth, migration, and invasion of breast cancer cells in vitro and synergizes with chemotherapeutic agents

OncoTargets and Therapy ◽

10.2147/ott.s148604 ◽

2017 ◽

Vol Volume 10 ◽

pp. 4869-4883 ◽

Cited By ~ 5

Author(s):

Nehad Ayoub ◽

Kamal Al-Shami ◽

Mohammad A Y Alqudah ◽

Nizar Mhaidat

Keyword(s):

Breast Cancer ◽

Cancer Cells ◽

Breast Cancer Cells ◽

Chemotherapeutic Agents ◽

Migration And Invasion ◽

Met Inhibitor

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Lycorine inhibits MDA-MB-231 breast cancer cell proliferation, migration and invasion that are associated with Wnt/β-catenin signaling

Bangladesh Journal of Pharmacology ◽

10.3329/bjp.v13i2.36350 ◽

2018 ◽

Vol 13 (2) ◽

pp. 192

Author(s):

Xia-Liang Chen

Keyword(s):

Breast Cancer ◽

Cancer Cells ◽

Breast Cancer Cells ◽

Video Clip ◽

Migration And Invasion ◽

Cancer Cell Proliferation ◽

Breast Cancer Cell Proliferation ◽

Full Screen ◽

Mtt Assays

This study was aimed to determine the effects of lycorine, a toxic crystalline alkaloid, on MDA-MB-231 breast cancer cells proliferation, migration and invasion, and to investigate the mechanism involved. The cells were cultured with different concentrations of lycorine in vitro. MTT assays were performed to determine the proliferation of cells. Transwell assays were performed to measure the migration and invasion of cells. The activation of Wnt/β-catenin signaling pathway and expression were assayed by Western blot. This study showed that proliferation, migration and invasion of MDA-MB-231 breast cancer cells could be inhibited by lycorine. Furthermore, we found that Wnt/β-catenin signaling was markedly blocked in MDA-MB-321 cells treated with lycorine. In conclusion, lycorine inhibits the proliferation, migration and invasion of MDA-MB-231 breast cancer cells that is associated with the suppression of Wnt/β-catenin signaling.Video Clip of Methodology:5 min 39 sec: <a href="https://www.youtube.com/v/JLgToa21Csc">Full Screen</a> <a href="https://www.youtube.com/watch?v=JLgToa21Csc">Alternate</a>

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Eupafolin Induces Apoptosis and Autophagy of Breast Cancer Cells Through PI3K/AKT, MAPKs and NF-κB Signaling Pathways

10.21203/rs.3.rs-571473/v1 ◽

2021 ◽

Author(s):

Jiahui Wei ◽

Yu Ding ◽

Xinmiao Liu ◽

Qing Liu ◽

Yiran Lu ◽

...

Keyword(s):

Breast Cancer ◽

Cancer Cells ◽

Cancer Cell ◽

Breast Cancer Cell ◽

Breast Cancer Cells ◽

Migration And Invasion ◽

Breast Cancer Cell Lines ◽

Cancer Cell Proliferation

Abstract Eupafolin is a flavonoid that can be extracted from common sage. Previous studies have reported that Eupafolin has antioxidant, anti-inflammatory and anti-tumor properties. However, no studies have investigated the role of Eupafolin in breast cancer. Herein, we investigated the effect of Eupafolin on two human breast cancer cell lines, as well as its potential mechanism of action. Next, the data showed that proliferation, migration and invasion ability of breast cancer cells that were treated with Eupafolin was significantly reduced, while the apoptosis rate was significantly increased. In addition, Eupafolin treatment caused breast cancer cell proliferation to be blocked in the S phase. Moreover, Eupafolin significantly induced autophagy in breast cancer cells, with an increase in the expression of LC3B-II/I. PI3K/AKT, MAPKs and NF-κB pathways were significantly inhibited by Eupafolin treatment. Additionally, 3-MA (a blocker of autophagosome formation) significantly reduced Eupafolin-induced activation of LC3B-II/I in breast cancer cells. Furthermore, Eupafolin displayed good in vitro anti-angiogenic activity. Additionally, anti-breast cancer activity of Eupafolin was found to be partially mediated by Cav-1. Moreover, Eupafolin treatment significantly weakened carcinogenesis of MCF-7 cells in nude mice. Therefore, this data provides novel directions on the use of Eupafolin for treatment of breast cancer.

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Pichia-Expressed Recombinant D6 and DARC Negatively Affect Cell Migration and Invasion of Breast Cancer Cells

Sains Malaysiana ◽

10.17576/jsm-2021-5010-15 ◽

2021 ◽

Vol 50 (10) ◽

pp. 3015-3033

Author(s):

Wee Yee Tan ◽

Boon Yin Khoo ◽

Ai Lan Chew

Keyword(s):

Breast Cancer ◽

Cell Migration ◽

Cell Viability ◽

Cancer Cells ◽

Cancer Cell ◽

Breast Cancer Cell ◽

Recombinant Proteins ◽

Breast Cancer Cells ◽

Migration And Invasion ◽

Cell Migration And Invasion

Atypical chemokine receptor proteins are termed ‘decoy proteins’ as their binding to the respective ligands does not lead to a typical signaling pathway but intercepts the action of chemokines. This method of chemokine activity regulation may also function in tumor suppression. D6 and DARC (Duffy Antigen Receptor for Chemokines) have been reported as decoy chemokine receptors in cancer studies. Purified Pichia-expressed D6 and DARC, produced in-house, were used in cell-based studies to test their biological activities. Cell viability tests showed that recombinant D6 and DARC did not affect cell viability significantly, suggesting that they were not involved in breast cancer cell death. Wound healing assays showed that the presence of recombinant D6 or DARC at 10 µg/mL optimally inhibited the migration of breast cancer cells. ELISA showed an inverse relationship between the recombinant proteins and CCL2 levels in the treated cells. Migration assay using Boyden chamber demonstrated the function of the recombinant proteins in inhibiting chemotaxis activity of treated cells. Invasion assay showed the ability of the recombinant proteins in inhibiting the invasion property of treated cells. Comparison of single and combinatorial effects of the recombinant proteins showed that the combination of D6 and DARC at a 1:1 ratio (10 µg/mL) is most effective in reducing CCL2 levels and inhibiting the migration and invasion of treated cells. It was shown that the purified Pichia-expressed recombinant D6 and DARC are the negative regulators of breast cancer cell migration and invasion, and the inhibition effects were greater when they were used in combination.

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