LINC00662 enhances cell progression and stemness in breast cancer by MiR-144-3p/SOX2 axis

An, Congjing; Hu, Z X; Li, Yuehong; Zhao, Pengxin; Liu, Runtian; Zhang, Qing; Zhu, Peiling; Li, Yanting; Wang, Ying

doi:10.1186/s12935-022-02576-0

Cited by 9 publications

(6 citation statements)

References 41 publications

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“…Our results have also shown that LINC00662 overexpression promotes some stem-like traits in GBC cells, including an increase in CD133 + /CD44 + cell populations and the expression of stemness-associated genes such as OCT4 and NANOG , which is strongly associated with greater aggressiveness in cancer cells [ 11 , 22 , 23 ]. These findings were similar to those found in breast cancer cell lines, where LINC00662 knockdown decreased the expression of OCT4 and NANOG, which decreased invasion, proliferation, and tumor growth, suggesting that this lncRNA could actively participate in the acquisition of the stem-like phenotype in breast cancer [ 24 ]. Another characteristic closely attributable to lncRNAs is the development of chemoresistance [ 25 , 26 ].…”

Section: Discussionsupporting

confidence: 84%

“…Interestingly, our in silico analyses showed that LINC00662 has two binding sites for miR-335-5p that could induce the repression of this miRNA, which was then confirmed in G-415 cells in which LINC00662 overexpression decreased miR-335-5p expression. Regarding this, similar studies showed that LINC00662 knockdown decreases the levels of OCT4 binding to miR-144-3p in breast cancer cells [ 24 ]. Since there were not significant differences in miR-335-5p levels between the control and LINC00662-transduced groups in GB-d1 cells, it is suggested that the oncogenic effects observed by LINC00662 overexpression could be through a different mechanism of regulation, which is very common among lncRNAs due to the large number of probable targets [ 40 ].…”

Section: Discussionmentioning

confidence: 93%

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LINC00662 Promotes Aggressive Traits by Modulating OCT4 Expression through miR-335-5p in Gallbladder Cancer Cells

Pérez-Moreno,

Riquelme,

Bizama

et al. 2024

IJMS

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Long non-coding RNAs (lncRNAs) are nucleotide sequences that participate in different biological processes and are associated with different pathologies, including cancer. Long intergenic non-protein-coding RNA 662 (LINC00662) has been reported to be involved in different cancers, including colorectal, prostate, and breast cancer. However, its role in gallbladder cancer has not yet been described. In this article, we hypothesize that LINC00662 has an important role in the acquisition of aggressiveness traits such as a stem-like phenotype, invasion, and chemoresistance in gallbladder cancer. Here, we show that LINC00662 is associated with larger tumor size and lymph node metastasis in patients with gallbladder cancer. Furthermore, we show that the overexpression of LINC00662 promotes an increase in CD133+/CD44+ cell populations and the expression of stemness-associated genes. LINC00662 promotes greater invasive capacity and the expression of genes associated with epithelial–mesenchymal transition. In addition, the expression of LINC00662 promotes resistance to cisplatin and 5-fluorouracil, associated with increased expression of chemoresistance-related ATP-binding cassette (ABC) transporters in gallbladder cancer (GBC) cell lines. Finally, we show that the mechanism by which LINC00662 exerts its function is through a decrease in microRNA 335-5p (miR-335-5p) and an increase in octamer-binding transcription factor 4 (OCT4) in GBC cells. Thus, our data allow us to propose LINC00662 as a biomarker of poor prognosis and a potential therapeutic target for patients with GBC.

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Section: Discussionsupporting

confidence: 84%

Section: Discussionmentioning

confidence: 93%

LINC00662 Promotes Aggressive Traits by Modulating OCT4 Expression through miR-335-5p in Gallbladder Cancer Cells

Pérez-Moreno,

Riquelme,

Bizama

et al. 2024

IJMS

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“…Such exo-lncRNAs have been implicated in the development, proliferation, invasion, angiogenesis, and drug resistance of tumors [ 10 ]. The LINC00662 gene, located on chromosome 19, encodes a 2085 bp lncRNA that is highly expressed in cancer, such as breast cancer and hepatocellular carcinoma [ 11 , 12 ]. Mechanistically, LINC00662 promotes tumor progression via interacting with both proteins and RNAs, as well as via regulating the Wnt/β-catenin, SMD and Hippo signaling pathways [ 13 ].…”

Section: Introductionmentioning

confidence: 99%

PITX1 suppresses osteosarcoma metastasis through exosomal LINC00662-mediated M2 macrophage polarization

Zhang

Chen

et al. 2022

Clin Exp Metastasis

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Paired-like homeodomain transcription factor 1 (PITX1) is frequently downregulated in cancers, including osteosarcoma (OS). However, its role in OS remains unknown. Therefore, we aimed to explore the functions and potential mechanisms of PITX1 in OS malignant progression. Elevated PITX1 suppressed OS cell proliferation and migration, based on transwell, proliferation, and colony formation assays. Pathway enrichment analysis of differentially-expressed genes between PITX1-overexpressing and control OS cells indicated that PITX1 expression was associated with the FAK/Src and PI3k/Akt signaling pathways. Mechanistically, ubiquitination assays and rescue experiments showed that PITX1 interacted with transcription factor STAT3, leading to decreased STAT3 transcriptional activity, which repressed the expression of LINC00662. Specific knockdown of LINC00662 reduced the tumor growth and invasion of OS cells induced by downregulated PITX1. Moreover, exosomal LINC00662, derived from PITX1 knockdown OS cell lines activated M2 macrophages in cell co-culture assays. M2 macrophage secreted several cytokines, among which CCL22 was found to cause OS cell EMT. Collectively, our data indicate that PITX1 suppresses OS cell proliferation and metastasis by downregulating LINC00662. Moreover, LINC00662 can be packaged into OS cell-derived exosomes to mediate M2 macrophage polarization to promote OS metastasis via CCL22.

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“…Fuso et al [ 87 ] reported that miR-100-5p modulates the PlK1 gene and Wnt/β-catenin pathway, acting as a pro-differentiating agent in BCSC. MiR-144-3p and miR-145-5p target SOX2 in BC cells and are involved in cell migration, invasion, stemness, and cancer progression [ 88 , 89 ]. The hERG gene, which is related to cell proliferation, differentiation, and apoptosis in several types of cancers, including BC, is targeted by miR-362-3p [ 90 ].…”

Section: Circulating Mirnas As Indicators Of Clinical Response To Nat...mentioning

confidence: 99%

Exploring the Potential Role of Circulating microRNAs as Biomarkers for Predicting Clinical Response to Neoadjuvant Therapy in Breast Cancer

Ruiz-Manriquez,

Villarreal-Garza,

Benavides-Aguilar

et al. 2023

IJMS

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Breast cancer (BC) is a leading cause of cancer-related deaths among women worldwide. Neoadjuvant therapy (NAT) is increasingly being used to reduce tumor burden prior to surgical resection. However, current techniques for assessing tumor response have significant limitations. Additionally, drug resistance is commonly observed, raising a need to identify biomarkers that can predict treatment sensitivity and survival outcomes. Circulating microRNAs (miRNAs) are small non-coding RNAs that regulate gene expression and have been shown to play a significant role in cancer progression as tumor inducers or suppressors. The expression of circulating miRNAs has been found to be significantly altered in breast cancer patients. Moreover, recent studies have suggested that circulating miRNAs can serve as non-invasive biomarkers for predicting response to NAT. Therefore, this review provides a brief overview of recent studies that have demonstrated the potential of circulating miRNAs as biomarkers for predicting the clinical response to NAT in BC patients. The findings of this review will strengthen future research on developing miRNA-based biomarkers and their translation into medical practice, which could significantly improve the clinical management of BC patients undergoing NAT.

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LINC00662 enhances cell progression and stemness in breast cancer by MiR-144-3p/SOX2 axis

Cited by 9 publications

References 41 publications

LINC00662 Promotes Aggressive Traits by Modulating OCT4 Expression through miR-335-5p in Gallbladder Cancer Cells

LINC00662 Promotes Aggressive Traits by Modulating OCT4 Expression through miR-335-5p in Gallbladder Cancer Cells

PITX1 suppresses osteosarcoma metastasis through exosomal LINC00662-mediated M2 macrophage polarization

Exploring the Potential Role of Circulating microRNAs as Biomarkers for Predicting Clinical Response to Neoadjuvant Therapy in Breast Cancer

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