LINC00173 promotes Wilms’ tumor progression through MGAT1-mediated MUC3A <i>N</i>-glycosylation

Zhu, Qingliang; Zhan, Deming; Yang, Yongguo; Chong, Yankun; Xue, Huadan; Zhu, Ping

doi:10.1080/15384101.2022.2070399

Cited by 7 publications

(5 citation statements)

References 46 publications

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“…A complex mechanism of glycosylation regulation by ncRNAs is provided by LINC00173, which promotes Wilms' tumor progression. LINC00173 stabilizes MGAT1 mRNA by recruiting the HNRPA2B1 ribonucleoprotein, resulting in mucin MUC3A Nglycosylation and tumor progression [81]. One of the hallmarks of Alzheimer's disease is the presence of a hyperphosphorylated form of tau protein, which is the basis of neurofibrillary tangle formation.…”

Section: N-linked Chainsmentioning

confidence: 99%

The Mutual Relationship between Glycosylation and Non-Coding RNAs in Cancer and Other Physio-Pathological Conditions

Duca

Malagolini

Dall’Olio

2022

IJMS

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Glycosylation, which consists of the enzymatic addition of sugars to proteins and lipids, is one of the most important post-co-synthetic modifications of these molecules, profoundly affecting their activity. Although the presence of carbohydrate chains is crucial for fine-tuning the interactions between cells and molecules, glycosylation is an intrinsically stochastic process regulated by the relative abundance of biosynthetic (glycosyltransferases) and catabolic (glycosidases) enzymes, as well as sugar carriers and other molecules. Non-coding RNAs, which include microRNAs, long non-coding RNAs and circRNAs, establish a complex network of reciprocally interacting molecules whose final goal is the regulation of mRNA expression. Likewise, these interactions are stochastically regulated by ncRNA abundance. Thus, while protein sequence is deterministically dictated by the DNA/RNA/protein axis, protein abundance and activity are regulated by two stochastic processes acting, respectively, before and after the biosynthesis of the protein axis. Consequently, the worlds of glycosylation and ncRNA are closely interconnected and mutually interacting. In this paper, we will extensively review the many faces of the ncRNA–glycosylation interplay in cancer and other physio-pathological conditions.

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Section: N-linked Chainsmentioning

confidence: 99%

The Mutual Relationship between Glycosylation and Non-Coding RNAs in Cancer and Other Physio-Pathological Conditions

Duca

Malagolini

Dall’Olio

2022

IJMS

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“…Furthermore, dysregulated expression lncRNAs are inextricably linked to tumorigenesis [ 24 ]. As shown in Table 1 , the high expression level of LINC00173 has been verified in several human cancers, including LC [ 17 , 25 , 26 , 27 , 28 ], hepatocellular carcinoma (HCC) [ 29 ], colorectal cancer (CRC) [ 30 ], ESCC [ 18 ], pancreatic cancer (PCA) [ 11 ], glioma [ 31 ], triple-negative breast cancer (TNBC) [ 32 ], prostate cancer (Pca) [ 33 ], and WT [ 34 ]. In contrast, LINC00173 is downregulated in cervical cancer (CC) [ 12 ], acute myeloid leukemia (AML) [ 35 ], and non-small cell lung cancer (NSCLC) [ 17 ].…”

Section: Aberrant Expression and Tumorigenesis Of Linc00173 In Human ...mentioning

confidence: 99%

“…WT is a kind of kidney cancer that occurs in childhood, and approximately one in 10,000 children suffer from WT [ 50 ]. Zhu et al [ 34 ] recently reported that LINC00173 was upregulated in WT cell lines more than that in the non-tumor human embryonic kidney cell lines. Furthermore, LINC00173 knockdown attenuated WT cell migration and invasion and enhanced apoptosis.…”

Section: Aberrant Expression and Tumorigenesis Of Linc00173 In Human ...mentioning

confidence: 99%

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Long Intergenic Non-Protein Coding RNA 173 in Human Cancers

Mao

Liao

Tang

2022

Cancers

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Long non-coding RNAs belong to non-coding RNAs (ncRNAs) with a length of more than 200 nucleotides and limited protein-coding ability. Growing research has clarified that dysregulated lncRNAs are correlated with the development of various complex diseases, including cancer. LINC00173 has drawn researchers’ attention as one of the recently discovered lncRNAs. Aberrant expression of LINC00173 affects the initiation and progression of human cancers. In the present review, we summarize the recent considerable research on LINC00173 in 11 human cancers. Through the summary of the abnormal expression of LINC00173 and its potential molecular regulation mechanism in cancers, this article indicates that LINC00173 may serve as a potential diagnostic biomarker and a target for drug therapy, thus providing novel clues for future related research.

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“…In contrast, it also suppresses tumorigenesis and tumor progression in lung adenocarcinoma [8], cervical cancer [9], and acute myeloid leukemia [10]. This cell context-dependent action of LINC00173 can be attributed to its varied molecular functions; it acts as a molecular sponge of miRNAs to stabilize the mRNAs and enhance the expression of target genes [7], and it selectively binds to target proteins, such as DNMT1 [10] and HNRNPA2B1 [11], to modulate their downstream pathways. This variety of LINC00173 molecular actions indicates that LINC00173 may have as yet undiscovered functions in other important biological processes.…”

Section: Introductionmentioning

confidence: 99%

Expression of Tumor Suppressor FHIT Is Regulated by the LINC00173-SNAIL Axis in Human Lung Adenocarcinoma

Suzuki,

Sakai,

Ota

et al. 2023

IJMS

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Long non-coding RNAs (lncRNAs) play a critical role in a variety of human diseases such as cancer. Here, to elucidate a novel function of a lncRNA called LINC00173, we investigated its binding partner, target gene, and its regulatory mechanism in lung adenocarcinoma, including the A549 cell line and patients. In the A549 cell line, RNA immunoprecipitation (RIP) assays revealed that LINC00173 efficiently binds to SNAIL. RNA-seq and RT-qPCR analyses revealed that the expression of FHIT was decreased upon LINC00173 depletion, indicating that FHIT is a target gene of LINC00173. Overexpression of SNAIL suppressed and depletion of SNAIL increased the expression of FHIT, indicating that SNAIL negatively regulates FHIT. The downregulation of FHIT expression upon LINC00173 depletion was restored by additional SNAIL depletion, revealing a LINC00173-SNAIL-FHIT axis for FHIT regulation. Data from 501 patients with lung adenocarcinoma also support the existence of a LINC00173-SNAIL-FHIT axis, as FHIT expression correlated positively with LINC00173 (p = 1.75 × 10−6) and negatively with SNAIL (p = 7.00 × 10−5). Taken together, we propose that LINC00173 positively regulates FHIT gene expression by binding to SNAIL and inhibiting its function in human lung adenocarcinoma. Thus, this study sheds light on the LINC00173-SNAIL-FHIT axis, which may be a key mechanism for carcinogenesis and progression in human lung adenocarcinoma.

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LINC00173 promotes Wilms’ tumor progression through MGAT1-mediated MUC3A N-glycosylation

Cited by 7 publications

References 46 publications

The Mutual Relationship between Glycosylation and Non-Coding RNAs in Cancer and Other Physio-Pathological Conditions

The Mutual Relationship between Glycosylation and Non-Coding RNAs in Cancer and Other Physio-Pathological Conditions

Long Intergenic Non-Protein Coding RNA 173 in Human Cancers

Expression of Tumor Suppressor FHIT Is Regulated by the LINC00173-SNAIL Axis in Human Lung Adenocarcinoma

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