scholarly journals MiR-486-3p inhibits the proliferation, migration and invasion of retinoblastoma cells by targeting ECM1

2020 ◽  
Vol 40 (6) ◽  
Author(s):  
Hongwei Yang ◽  
Yonggang Huang ◽  
Jian He ◽  
Guangrui Chai ◽  
Yu Di ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Target Genes ◽  
Inhibitory Effect ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Retinoblastoma Cells ◽  
Tumor Tissues ◽  
Regulatory Effects ◽  
Related Proteins

Abstract It has been reported that miR-486-3p expression is decreased in retinoblastoma (RB) tumor tissues, however, its function in RB has been less reported. The present study aimed to explore the regulatory effects of miR-486-3p on RB cells. The expression of miR-486-3p in RB tissues and cells was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability, proliferation, apoptosis, migration and invasion ability were determined by cell counting kit-8 (CCK-8) kit, clone formation assay, flow cytometry, scratch assay and transwell, respectively. Targetscan 7.2 and dual-luciferase reporter were used to verify target genes for miR-486-3p. The expressions of apoptosis-related proteins and ECM1 were detected by Western blot. The miR-486-3p expression was decreased in RB tissues and cells. In RB cells, overexpression of miR-486-3p inhibited cell proliferation, migration and invasion, while promoted apoptosis. Moreover, overexpression of miR-486-3p decreased Bcl-2 expression, while increased the expressions of Bax and Cleaved Caspase-3 (C caspase-3). ECM1 was the target gene of miR-486-3p, and miR-486-3p inhibited the expression of ECM1. Furthermore, ECM1 partially reversed the inhibitory effect of miR-486-3p on the proliferation, migration and invasion of RB cells. MiR-486-3p inhibited the proliferation, migration and invasion of RB by down-regulating ECM1.

scholarly journals MicroRNA-573 inhibits cell proliferation, migration and invasion and is downregulated by PICSAR in cutaneous squamous cell carcinoma

2021 ◽  
Author(s):  
Yanhua Wang ◽  
Shengjian Tang ◽  
Jianping Lv
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Cutaneous Squamous Cell Carcinoma ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Tumor Tissues ◽  
Regulatory Effects

The incidence of cutaneous squamous cell carcinoma (cSCC) has been increasing in recent years. Meanwhile, microRNAs (miRNAs) have been found to play vital roles in various cancers, including cSCC. This study aimed to investigate the expression of microRNA-573 (miR-573) in cSCC, its relationship with long non-coding RNA PICSAR and analyze its biological role. The relationship between PICSAR and miR-573 was confirmed by dual-luciferase reporter assay and Pearson’s correlation coefficient analysis. The levels of PICSAR and miR-573 were measured using quantitative Real-Time PCR. Cell Counting Kit-8 assay was used to evaluate the cSCC cell proliferation ability. The migration and invasion abilities of cSCC cells were evaluated by Transwell assay. PICSAR expression was increased and miR-573 was decreased in tumor tissues and cSCC cell lines. PICSAR and miR-573 can bind directly, and miR-573 expression was downregulated by PICSAR in cSCC. Overexpression of miR-573 significantly inhibited the proliferation, migration and invasion abilities of A431 and SCC13 cells. Additionally, miR-573 overexpression reversed the promotion effects of PICSAR overexpression on cSCC cell proliferation, migration and invasion abilities. In conclusion, our findings indicated that miR-573 expression was decreased in tumor tissues and cSCC cells and was downregulated by PICSAR in cSCC. Additionally, miR-573 overexpression inhibited cSCC cell proliferation, migration and invasion, and reversed the promotion effects of PICSAR overexpression on cSCC cell biological functions. Thus, miR-573 might function as a tumor suppressor and might be involved in the regulatory effects of PICSAR on tumorigenesis in cSCC.

scholarly journals LncRNA SNHG16 Contributes to Tumor Progression via miR-302b-3p/SLC2A4 in Pancreatic Cancer

2020 ◽  
Author(s):  
Hao Xu ◽  
Xin Miao ◽  
Xin Li ◽  
Haofei Chen ◽  
Bo Zhang ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Caspase 3 ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Caspase 9 ◽  
Transwell Assay ◽  
Qrt Pcr ◽  
Rna Immunoprecipitation ◽  
Related Proteins ◽  
Dual Luciferase Reporter Assay

Abstract Background: It is reported that lncRNA SNHG16 is significantly highly expressed in pancreatic cancer (PC). However, the functions and mechanisms of SNHG16 are not clear. The aim of this study was to explore the effects of SNHG16 in PC.Methods: qRT-PCR analyze was applied to detect the expression levels of SNHG16, miR-302b-3p and SLC2A4 in PC tissues and cells. CCK8 and EdU assays were used to determine the proliferation of PC cells. Transwell assay were used to measure the capacities of PC cells migration and invasion. Apoptosis were evaluated by flow cytometry, and the expression of apoptosis related proteins (including Bax, Bcl-2, cleaved caspase-3 and cleaved caspase-9), which were tested by western blot. The interactions between miR-302b-3p and SNHG16 or miR-302b-3p and SLC2A4 mRNA 3’UTR were clarified by Dual luciferase reporter assay and RNA immunoprecipitation.Results: SNHG16 was significantly elevated in PC tissues and cell lines, which was associated with poor prognosis of PC patients. Knockdown of SNHG16 reduced PC cells proliferation, migration and invasion. SNHG16 acted as a sponge to regulate miR-302b-3p expression in PC cells. And miR-302b-3p targeted SLC2A4 directly. Conclusions: SNHG16 promoted the progression of PC via miR-302b-3p/SLC2A4 axis and was expected to be a potential target for early diagnosis and treatment of PC.

scholarly journals Long non-coding RNA LINC00488 facilitates thyroid cancer cell progression through miR-376a-3p/PON2

2021 ◽  
Vol 41 (3) ◽  
Author(s):  
Fuyuan Xie ◽  
Longgen Li ◽  
Yuting Luo ◽  
Rensheng Chen ◽  
Jinhong Mei
Keyword(s):  
Thyroid Cancer ◽  
Cancer Cell ◽  
Target Gene ◽  
Target Genes ◽  
Bioinformatics Analysis ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Thyroid Cancer Cell ◽  
Gene Assay

Abstract Objective: Long non-coding RNAs (lncRNAs) recently have been identified as influential indicators in a variety of malignancies. The aim of the present study was to identify a functional lncRNA LINC00488 and its effects on thyroid cancer in the view of cell proliferation and apoptosis. Methods: In order to evaluate the effects of LINC00488 on the cellular process of thyroid cancer, we performed a series of in vitro experiments, including cell counting kit-8 (CCK-8) assay, EdU (5-ethynyl-2′-deoxyuridine) assay, flow cytometry, transwell chamber assay, Western blot and RT-qPCR. The target gene of LINC00488 was then identified by bioinformatics analysis (DIANA and TargetScan). Finally, a series of rescue experiments was conducted to validate the effect of LINC00488 and its target genes on proliferation, migration, invasion and apoptosis of thyroid cancer. Results: Our findings revealed that LINC00488 was highly expressed in thyroid cancer cell lines (BCPAP, BHP5-16, TPC-1 and CGTH-W3) and promoted the proliferation, migration and invasion, while inhibited the apoptosis of thyroid cancer cells (BCPAP and TPC-1). The results of bioinformatics analysis and dual luciferase reporter gene assay showed that LINC00488 could directly bind to miR-376a-3p and down-regulated the expression level of miR-376a-3p. In addition, Paraoxonase-2 (PON2) was a target gene of miR-376a-3p and negatively regulated by miR-376a-3p. Rescue experiment indicated that LINC00488 might enhance PON2 expression by sponging miR-376a-3p in thyroid cancer. Conclusion: Taken together, our study revealed that lncRNA LINC00488 acted as an oncogenic gene in the progression of thyroid cancer via regulating miR-376a-3p/PON2 axis, which indicated that LINC00488-miR-376a-3p-PON2 axis could serve as novel biomarkers or potential targets for the treatment of thyroid cancer.

LncRNA MAFG-AS1 Promotes the Progression of Bladder Cancer by Targeting the miR-143-3p/COX-2 Axis

Pathobiology ◽  
2020 ◽  
Vol 87 (6) ◽  
pp. 345-355
Author(s):  
Dengbao Li ◽  
Siwen Zhong ◽  
Zhiqiang Zhu ◽  
Xinan Jiang ◽  
Junhao Zhang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Cell Lines ◽  
Biological Effects ◽  
Histological Grade ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Cox 2 ◽  
Regulatory Effects

<b><i>Background:</i></b> Long noncoding RNAs (lncRNAs) are potential biomarkers that are very important for the development of cancer. Studies show that lncRNAs are significantly correlated with the carcinogenesis and progression of bladder cancer (BLCA). In this research, we aimed at probing into the role of lncRNA MAFG-AS1 in the tumorigenesis of BLCA. <b><i>Methods:</i></b> RT-qPCR was employed to detect MAFG-AS1 expression in BLCA tissues and cells. MAFG-AS1 siRNA and overexpression plasmid were transfected into 5637 and T24 BLCA cell lines to inhibit or upregulate MAFG-AS1 expression, respectively, and then the regulatory functions of MAFG-AS1 on BLCA cell proliferation, migration, and invasion were assessed using cell counting kit-8 (CCK-8) assay, EdU method, and Transwell experiments, respectively. Dual-luciferase reporter assay and RNA immunoprecipitation were conducted to validate the targeting relationships between MAFG-AS1 and miR-143-3p, and miR-143-3p and COX-2. In addition, miR-143-3p was repressed in MAFG-AS1-silenced 5637 and T24 cell lines, and the function of MAFG-AS1/miR-143-3p axis in BLCA cells was further evaluated. The regulatory effects of MAFG-AS1 and miR-143-3p on the expression of COX-2 protein were detected by Western blot. <b><i>Results:</i></b> MAFG-AS1 was remarkably upregulated in BLCA patient tissues and cell lines, and its high expression was closely related to histological grade, tumor size, and lymph node metastasis. Silencing of MAFG-AS1 inhibited BLCA cell proliferation, metastasis, and invasion, while overexpression of MAFG-AS1 in BLCA cells had opposite biological effects. MAFG-AS1 was proved to target miR-143-3p to repress its expression. Moreover, it was confirmed that MAFG-AS1 and miR-143-3p could modulate COX-2 expression. <b><i>Conclusion:</i></b> The MAFG-AS1/miR-143-3p/COX-2 axis contributes to BLCA progression.

scholarly journals Long non-coding RNA PVT1-mediated miR-543/SERPINI1 axis plays a key role in the regulatory mechanism of ovarian cancer

2020 ◽  
Vol 40 (6) ◽  
Author(s):  
Chong Qu ◽  
Chunmei Dai ◽  
Yahua Guo ◽  
Rui Qin ◽  
Junbao Liu
Keyword(s):  
Ovarian Cancer ◽  
Cell Lines ◽  
Target Genes ◽  
Inhibitory Effect ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Regulation Mechanism ◽  
Regulatory Relationship ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Abstract Purpose: To investigate the regulation mechanism of long non-coding RNA (lncRNA) plasmocytoma variant translocation 1 (PVT1) in ovarian cancer (OC). Methods: The levels of PVT1, microRNA (miR)-543, serpin peptidase inhibitor-clade I (neuroserpin)-member 1 (SERPINI1) in OC tissues and OVCAR-3, A2780, TOV-112D of OC cell lines were detected by quantitative real-time PCR (qRT-PCR) and Western Blot (WB). Cell proliferation, migration, invasion, apoptosis and the regulatory relationship between genes and target genes were analyzed by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), Transwell, flow cytometry and dual luciferase reporter (DLR). The OC patients were followed up for 5 years to analyze the relationship between PVT1 and 5-year overall survival (OS). Results: In contrast with miR-543, PVT1 and SERPINI1 were highly expressed in OC tissues and cell lines, and high levels of PVT1 were significantly associated with lower 5-year OS of patients. Down-regulating PVT1 not only inhibited the malignant proliferation, migration and invasion of OC cells, but promoted cell apoptosis. PVT1 regulated miR-543 in a targeted manner, and its overexpression could attenuate the anticancer effect of miR-543 on OC cells. In addition, miR-543 also directly targeted SERPINI1, and miR-543 knockdown weakened the inhibitory effect of down-regulated SERPINI1 on OC progression. Furthermore, we found that PVT1 acted as a competitive endogenous RNA to sponge miR-543, thereby regulating the expression of SERPINI1. Conclusion: PVT1 can mediate the molecular mechanism of OC by miR-543/SERPINI1 axis regulatory network, which is a new therapeutic direction for OC.

scholarly journals LncRNA-KCNQ1OT1: A Potential Target in Exosomes Derived From ADSCs for The Treatment of Osteoporosis

2021 ◽  
Author(s):  
Shanzheng Wang ◽  
Jun Jia ◽  
Chang-hong Chen
Keyword(s):  
Caspase 3 ◽  
Osteoporosis Treatment ◽  
Underlying Mechanism ◽  
Inhibitory Effect ◽  
Luciferase Reporter Assay ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Reporter Assay ◽  
Tnf Α ◽  
Factor Α

Abstract Background Osteoporosis is a worldwide medical and socioeconomic threat characterized by systemic impairment to bone strength and microstructure. Exosomes derived from adipose-derived stem cells (ADSCs-Exos) have been confirmed to play effective roles in the repair of various tissues and organs. This study aimed to investigate the role of ADSCs-Exos and a noval long none coding RNAKCNQ1OT1 (lnc-KCNQ1OT1) played in osteoporosis as well as the underlying mechanism. Methods MC3T3-E1 cells were treated with different doses of TNF-α (0, 1, 2.5, 5, 10 ng/ml) and then co-cultured with ADSCs-Exos or exosomes-derived from lnc-KCNQ1OT1-modified ADSCs (KCNQ1OT1-Exos). The expression of microRNA (miRNA)-141-5p (miR-141-5p) and lnc-KCNQ1OT1 was evaluated by quantitative real-time polymerase chain reaction (qRT-PCR). The protein expression of cleaved-caspase-3, caspase-3 and Bax was determined by Western blot. Cell viability and apoptosis were assessed by cell counting kit 8 (CCK-8) and flow cytometry analysis, respectively. The binding sites between KCNQ1OT1 and miR-141-5p were validated by dual-luciferase reporter assay. Results Tumor necrosis factor-α (TNF-α) dose dependently increased miR-141-5p expression, inhibited viability and promoted apoptosis of MC3T3-E1 cells. However, miR-141-5p silencing or co-culture with ADSCs-Exos attenuated these effects. In addition, KCNQ1OT1-Exos could more significantly attenuate the induced cytotoxicity and apoptosis compared to ADSCs-Exos. Moreover, miR-141-5p was confirmed as the target of lnc-KCNQ1OT1 by luciferase reporter assay. Conclusions ADSCs-Exos attenuated cytotoxicity and apoptosis of TNF-α-induced MC3T3-E1 cells. KCNQ1OT1-Exos had a more significant inhibitory effect compared to ADSCs-Exos by the function of sponging miR-141-5p, suggesting that KCNQ1OT1-Exos could be promising agents in osteoporosis treatment.

scholarly journals MicroRNA-133b Inhibits nTumor Cell Proliferation, Migration and Invasion by Targeting SUMO1 in Endometrial Carcinoma

2021 ◽  
Vol 20 ◽  
pp. 153303382110652
Author(s):  
Lingyun Liao ◽  
Yun Chen ◽  
Jieli Zhou ◽  
Jing Ye
Keyword(s):  
Cell Proliferation ◽  
Tumor Suppressor ◽  
Endometrial Carcinoma ◽  
Target Genes ◽  
Menopausal Status ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Functional Assay ◽  
Ec Cells

Objectives: An increasing number of studies have confirmed that microRNAs (miRNAs/miRs), as oncogenes or tumor suppressor genes, play an important regulatory role in the occurrence and development of numerous types of cancer. The aim of the present study was to investigate the potential role and mechanism of miR-133b and small ubiquitin like modifier 1 (SUMO1) in the development of endometrial carcinoma (EC). Methods: First, Venn diagrams are used to identify the differential expressions of miRNAs in EC from GSE35794 and GSE25405 datasets. Next, we conduct a series of functional tests, including Cell Counting Kit-8, wound healing, and transwell and matrigel assays. Then, a bioinformatics tool, is used to identify downstream target genes of miR-133b and to verify the predicted results by RT-qPCR, Western blotting and double luciferase reporter gene analysis. Finally, in order to further study whether the cellular function of miR-133b is mediated by the expression of SUMO1, rescue experiments were carried out. Results: The results of bioinformatics studies showed that the expression of miR-133b was down-regulated in EC tissues, and the expression level of miR-133b was lower in patients with high grade, different histology or menopausal status. The results of functional assay showed that overexpression of miR-133b reduced cell proliferation, migration and invasion. On the contrary, miR-133b silence has the opposite effect. SUMO1 was the direct target of miR-133b and was negatively regulated by miR-133b. The decrease of SUMO1mRNA expression inhibited the proliferation, migration and invasion of EC cells, and reversed the effect of miR-133b on EC cells. Conclusion: The findings from the present study suggested that miR-133b may be a tumor suppressor gene and a potential therapeutic target for the treatment of EC.

scholarly journals MicroRNA-29a Inhibits Growth, Migration and Invasion of Melanoma A375 Cells in Vitro by Directly Targeting BMI1

2018 ◽  
Vol 50 (1) ◽  
pp. 385-397 ◽  
Author(s):  
Ying Xiong ◽  
Liqian Liu ◽  
Ying Qiu ◽  
Lili  Liu
Keyword(s):  
Cell Viability ◽  
Cell Lines ◽  
Target Gene ◽  
Target Genes ◽  
Malignant Tumors ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Bmi1 Expression ◽  
A375 Cells

Background/Aims: Melanoma is one of the most aggressive malignant tumors, with increasing incidence, poor prognosis, and lack of any effective targeted therapies. Abnormal expression of miR-29a has been found in several types of cancers, including melanoma. In this study, experiments were performed to investigate the role of miR-29a in melanoma, and the molecular mechanism by which miR-29a represses melanoma. Methods: miR-29 and Bmi1 expression was examined by quantitative real-time polymerase chain reaction (qRT-PCR). The cell viability, apoptosis, migration and invasion were respectively determined by Cell Counting Kit-8 assay, Propidium iodide (PI) fluorescein isothiocynate (FITC)-Annexin V staining assay, wound healing assay and transwell assay. Luciferase reporter assay was performed to determine a target gene of miR-29a. Western blot was used to analyze protein expression of apoptosis-related proteins, Bmi1, Wnt/β-catenin and Nuclear factor-κB (NF-κB) pathway target genes. Results: miR-29a was down-regulated in all tested melanoma cell lines. Up-regulation of miR-29a effectively inhibited cell viability, migration, and invasion, but promoted apoptosis in A375 cells. Bmi1 was a direct target gene of miR-29a. Transfection with miR-29a mimic decreased cell migration and invasion and Bmi1 expression in Malme-3M cells, SK-MEL-2, SK-MEL-5, and M14 cell lines. Moreover, miR-29a might suppress growth, migration and invasion of A375 cells by negatively regulating Bmi1. In addition, our results demonstrated that transfection with miR-29a mimic effectively blocked Wnt/β-catenin and NF-κB pathways via down-regulating Bmi1. Conclusion: miR-29a could be functioned as a potential tumor suppressor through direct regulation of Bmi1 in melanoma cells.

scholarly journals LncRNA SNHG16 contributes to tumor progression via the miR-302b-3p/SLC2A4 axis in pancreatic adenocarcinoma

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Hao Xu ◽  
Xin Miao ◽  
Xin Li ◽  
Haofei Chen ◽  
Bo Zhang ◽  
...  
Keyword(s):  
Pancreatic Adenocarcinoma ◽  
Caspase 3 ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Pcr Analysis ◽  
Caspase 9 ◽  
Qrt Pcr ◽  
Rna Immunoprecipitation ◽  
Related Proteins ◽  
Dual Luciferase Reporter Assay

Abstract Background It has been reported that the lncRNA SNHG16 has significantly increased expression in pancreatic adenocarcinoma (PC). However, the functions and mechanisms of SNHG16 are not clear. The aim of this study was to explore the effects of SNHG16 on PC. Methods qRT-PCR analysis was applied to detect the expression levels of SNHG16, miR-302b-3p and SLC2A4 in PC tissues and cells. CCK8 and EdU assays were used to evaluate the proliferation of PC cells. Transwell assays were used to assess PC cell migration and invasion. Apoptosis was evaluated by flow cytometry, and the expression of apoptosis-related proteins (including Bax, Bcl-2, cleaved caspase-3 and cleaved caspase-9) was tested by western blotting. The interactions between miR-302b-3p and SNHG16 or miR-302b-3p and the 3’UTR of SLC2A4 mRNA were clarified by a dual luciferase reporter assay and RNA immunoprecipitation. Results SNHG16 expression was significantly elevated in PC tissues and cell lines and was associated with poor prognosis of PC patients. Knockdown of SNHG16 reduced PC cell proliferation, migration and invasion. SNHG16 acted as a sponge to regulate miR-302b-3p expression in PC cells. In addition, miR-302b-3p targeted SLC2A4 directly. Conclusions SNHG16 promoted the progression of PC via the miR-302b-3p/SLC2A4 axis and was expected to be a potential target for the early diagnosis and treatment of PC.

scholarly journals CircWHSC1 Promotes Breast Cancer Progression by Regulating the FASN/AMPK/mTOR Axis Through Sponging miR-195-5p

2022 ◽  
Vol 11 ◽  
Author(s):  
Qian Chen ◽  
Zhen Yang ◽  
Hongjian Ding ◽  
Huaqing Li ◽  
Weiyu Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Progression ◽  
Fatty Acid Synthase ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Circular Rnas ◽  
Ampk Pathway ◽  
Tumor Tissues ◽  
Tumor Stages

Numerous studies reveal that circular RNAs (circRNAs) affect cancer progression. CircWHSC1 is a novel circRNA that accelerates ovarian cancer progression. Nevertheless, the function of circWHSC1 in regulating breast cancer (BC) is elusive. Here, quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was carried out to detect the profiles of circWHSC1 and miR-195-5p in BC tissues and corresponding non-tumor tissues. Gain- and loss-of-function assays were implemented both in vivo and ex vivo to verify the significance of circWHSC1 in BC development. BC cell proliferation was estimated by the cell counting kit-8 (CCK-8) and BrdU assays. Transwell assay was implemented to test BC cell migration and invasion. The protein levels of FASN, AMPK and mTOR were determined by Western blot. Moreover, immunohistochemistry was performed to examine Ki67 and FASN expression. As shown by the result, circWHSC1 was up-regulated in BC tissues versus adjacent non-tumor tissues. circWHSC1 overexpression was correlated with higher tumor stages, lymphatic metastasis and worse survival of BC patients. Functionally, overexpressing circWHSC1 amplified proliferation, migration and invasion of BC cell lines and boosted xenograft tumor growth in nude mice. Bioinformatics uncovered that circWHSC1 functioned as a competitive endogenous RNA by sponging miR-195-5p, which was further corroborated by the dual-luciferase reporter assay and RNA immunoprecipitation. miR-195-5p delayed BC progression, which was dampened by circWHSC1 up-regulation. Fatty acid synthase (FASN) was affirmed as a direct target of miR-195-5p. miR-195-5p overexpression curbed FASN expression and activated its downstream AMPK pathway. Inhibition of FASN or activation of the AMPK pathway reversed circWHSC1-mediated oncogenic effects. Collectively, CircWHSC1 acted as an oncogene to expedite BC evolvement by modulating the miR-195-5p/FASN/AMPK/mTOR pathway.

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