miR-204/COX5A axis contributes to invasion and chemotherapy resistance in estrogen receptor-positive breast cancers

Zeng, Jin; Li, Guoli; Xia, Yan; Wang, Fengping; Wang, Yanzhong; Xu, Shoufang; Zhou, Yixuan; Liu, Xiyong; Xie, Xinyou; Zhang, Jun

doi:10.1016/j.canlet.2020.07.027

Cited by 16 publications

(18 citation statements)

References 49 publications

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“…Cervical cancer, as one of the common human tumors, is one of the most common gynecological malignancies, [1][2][3][4][5]34 which is like other tumors [35][36][37][38][39][40][41] and they threatened seriously to human health as well as cervical cancer, [42][43][44][45][46][47][48] its morbidity and mortality rate are at the forefront of female malignancies. Surgery, radiotherapy and chemotherapy for early cervical cancer have good effects, but in advanced stage, the therapeutic effect of metastatic and recurrent cervical cancer is very limited and the survival rate is low.…”

Section: Discussionmentioning

confidence: 99%

“…The encoded protein plays a central role in high-density lipoprotein (HDL) and very low-density lipoprotein (VLDL) metabolism. 47 According to the results of previous studies, APOC1 was involved in the progression and development of various cancers. APOC1 was abnormally expressed in gastric cancer (GC), colorectal cancer (CRC), prostate cancer (PCa), lung cancer, pancreatic cancer, renal cancer and so on.…”

Section: Dovepressmentioning

confidence: 99%

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<p>Apolipoprotein C1 (APOC1): A Novel Diagnostic and Prognostic Biomarker for Cervical Cancer</p>

Shi¹,

Wang²,

Dai³

et al. 2020

OTT

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Background Previous reports showed that APOC1 was associated with several cancers but the function of APOC1 in cervical cancer was unknown. This study aimed to investigate the clinical effect and function of APOC1 in cervical cancer. Materials and Methods In this study, the relative expression of APOC1 in cervical cancer was detected by RT-qPCR. In order to determine the cell proliferation and migration and invading ability and apoptosis more accurately, we used CCK8 assay, Edu assay, wound healing assay, migration and invasion assay, flow cytometry assay, co-immunoprecipitation, proteomics and Western blot by silencing and overexpressing APOC1 , respectively. The role of APOC1 on tumor progression was explored in vitro and vivo. Results The relative expression of APOC1 in cervical cancer tissues was up-regulated (P<0.05). In cervical cancer cell lines, silencing of APOC1 restrained cell progression and EMT, while over-expression of APOC1 accelerated cell progression and EMT in vivo and vitro (P<0.05). Conclusion APOC1 acts as an oncogene in cervical cancers and knockdown of APOC1 inhibited cervical cancer cells growth in vitro and in vivo. There is a close relationship between the relative expression of APOC1 and clinical outcome in cervical cancer patients.

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Section: Discussionmentioning

confidence: 99%

Section: Dovepressmentioning

confidence: 99%

<p>Apolipoprotein C1 (APOC1): A Novel Diagnostic and Prognostic Biomarker for Cervical Cancer</p>

Shi¹,

Wang²,

Dai³

et al. 2020

OTT

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“…More importantly, COX5A, NDUFAB1, SDHB, UQCRC2, and UQCRFS1 were selected as hub genes, and the downregulation of these genes is supposed to be vitally causative of AD. COX5A is the nuclear genome-encoded subunit Va of cytochrome c oxidase (COX or complex IV), which is indispensable in the regulation and assembly of mitochondrial respiratory chain holoenzyme [ 61 , 62 ]. Previous studies have shown that mitochondrial COX activity in AD brains is dramatically decreased, an early alteration of bioenergetic dysfunction closely related to cognitive decline [ 63 , 64 ].…”

Section: Discussionmentioning

confidence: 99%

Molecular Signatures of Mitochondrial Complexes Involved in Alzheimer’s Disease via Oxidative Phosphorylation and Retrograde Endocannabinoid Signaling Pathways

Chen

Bai

Zhong

et al. 2022

Oxidative Medicine and Cellular Longevity

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Objective. The inability to intervene in Alzheimer’s disease (AD) forces the search for promising gene-targeted therapies. This study was aimed at exploring molecular signatures and mechanistic pathways to improve the diagnosis and treatment of AD. Methods. Microarray datasets were collected to filter differentially expressed genes (DEGs) between AD and nondementia controls. Weight gene correlation network analysis (WGCNA) was employed to analyze the correlation of coexpression modules with AD phenotype. A global regulatory network was established and then visualized using Cytoscape software to determine hub genes and their mechanistic pathways. Receiver operating characteristic (ROC) analysis was conducted to estimate the diagnostic performance of hub genes in AD prediction. Results. A total of 2,163 DEGs from 13,049 background genes were screened in AD relative to nondementia controls. Among the six coexpression modules constructed by WGCNA, DEGs of the key modules with the strongest correlation with AD were extracted to build a global regulatory network. According to the Maximal Clique Centrality (MCC) method, five hub genes associated with mitochondrial complexes were chosen. Further pathway enrichment analysis of hub genes, such as oxidative phosphorylation and retrograde endocannabinoid signaling, was identified. According to the area under the curve (AUC) of about 70%, each hub gene exhibited a good diagnostic performance in predicting AD. Conclusions. Our findings highlight the perturbation of mitochondrial complexes underlying AD onset, which is mediated by molecular signatures involved in oxidative phosphorylation (COX5A, NDUFAB1, SDHB, UQCRC2, and UQCRFS1) and retrograde endocannabinoid signaling (NDUFAB1) pathways.

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“…Accounting studies demonstrated that misregulated miRNAs work as tumor suppressors or promoters participating in the pathogenesis of many cancers [24]. Several researchers focused on the role of miRNAs in tumorigenesis and tumor progression and found that miR-204, an important tumor-suppressive miRNA, repressed the expression of oncogene targets and thus suppressed the growth and metastasis of cancer cells in many tumors, such as colorectal cancer, endometrial carcinoma, and breast cancer [25][26][27]. A previous study proved that miR-204 is downregulated in PTC cells and tissues.…”

Section: Discussionmentioning

confidence: 99%

Fentanyl Exerts an Antitumor Effect on Papillary Thyroid Cancer by Regulating the miR-204/KLF5 Axis

Jiang

Dai

et al. 2021

Journal of Nanomaterials

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Fentanyl is a strong anesthetic analgesic drug that plays important roles in many types of cancers. However, the role of fentanyl in papillary thyroid cancer (PTC) tumor development remains ambiguous. In this study, we aimed to investigate the potential antitumor effects of fentanyl on PTC cell viability and invasion. Results of cell counting kit-8 and Transwell assays demonstrated that fentanyl treatment (5 ng/ml) reduced the viability and invasion of two PTC cells, TCP-1 and BCPAP. Our data subsequently showed that fentanyl induced antitumor effects by increasing miR-204 expressions. Furthermore, the results of luciferase reporter assays identified that miR-204 directly targets Krüppel-like transcription factor 5 (KLF5), which serves as tumor-promoting genes in many cancers. Further mechanistic analyses revealed that fentanyl performs its tumor-suppressive functions by regulating the miR-204/KLF5 axis in PTC cells. These results contribute to understanding the important role of fentanyl in treating PTC.

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miR-204/COX5A axis contributes to invasion and chemotherapy resistance in estrogen receptor-positive breast cancers

Cited by 16 publications

References 49 publications

<p>Apolipoprotein C1 (APOC1): A Novel Diagnostic and Prognostic Biomarker for Cervical Cancer</p>

<p>Apolipoprotein C1 (APOC1): A Novel Diagnostic and Prognostic Biomarker for Cervical Cancer</p>

Molecular Signatures of Mitochondrial Complexes Involved in Alzheimer’s Disease via Oxidative Phosphorylation and Retrograde Endocannabinoid Signaling Pathways

Fentanyl Exerts an Antitumor Effect on Papillary Thyroid Cancer by Regulating the miR-204/KLF5 Axis

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