<scp>MYCT</scp>1 represses apoptosis of laryngeal cancerous cells through the <scp>MAX</scp>/miR‐181a/<scp>NPM</scp>1 pathway

Wang, Hetan; Xue, Ting; Zhang, Zhao-Xiong; Sun, Yuanyuan; Yan, Wei; Xu, Zhonghua; Fu, Wei‐Neng

doi:10.1111/febs.14942

Cited by 22 publications

(13 citation statements)

References 45 publications

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“…For instance, miR-181a-5p expression is lowered in prostate cancer, and up-regulated expression of miR-181a-5p in vitro can suppress cell proliferation and induce cell cycle arrest [ 44 ]. Importantly, miR-181a-5p can inhibit GATA6 expression, thereby inhibiting LSCC cell migration and inducing the apoptosis [ 45 ]; miR-181a-5p also induces LSCC cell apoptosis and inhibits the proliferation and colony formation by targeting NPM1, thus inhibiting LSCC progression [ 46 ]. This study confirmed that miR-181a-5p was a downstream target of LINC00847.…”

Section: Discussionmentioning

confidence: 99%

Long intergenic non-protein coding RNA 847 promotes laryngeal squamous cell carcinoma progression through the microRNA-181a-5p/zinc finger E-box binding homeobox 2 axis

XiaoLin

2022

Bioengineered

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The present study is targeted at investigating the effects of long intergenic non-protein coding RNA 847 (LINC00847) on the malignant biological behaviors of laryngeal squamous cell carcinoma (LSCC) cells, and the mechanisms. Quantitative real-time PCR and Western blotting were conducted for detecting the expressions of LINC00847, microRNA-181a-5p (miR-181a-5p) and zinc finger E-box binding homeobox 2 (ZEB2) in LSCC cell lines and tissue samples. BrdU, cell counting kit-8, scratch wound healing, Transwell and flow cytometry assays were utilized for detecting cell proliferation, migration, invasion, and cell cycle progression. Dual-luciferase reporter gene, RNA binding protein immunoprecipitation (RIP), and RNA pull-down assays were utilized to investigate the interaction among LINC00847, miR-181a-5p, and ZEB2. The subcellular location of LINC00847 was determined by RNA fluorescence in situ hybridization (RNA-FISH) assay. Tumor growth was evaluated using a xenograft model of nude mice. It was revealed that LINC00847 expression was increased in LSCC tissues, and its high expression was associated with lymph node metastasis and poor differentiation. LINC00847 was mainly located in the cytoplasm of LSCC cells, and LINC00847 overexpression promoted LSCC cell proliferation, migration, invasion, and accelerated the cell cycle progression while knocking down LINC00847 had the opposite effects in vitro and inhibited the tumor growth in vivo . LINC00847 directly targeted miR-181a-5p and negatively modulated miR-181a-5p expression. ZEB2 was a target gene of miR-181a-5p, and was positively and indirectly modulated by LINC00847. Our data suggest that LINC00847 promotes LSCC progression by regulating the miR-181a-5p/ZEB2 axis.

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Section: Discussionmentioning

confidence: 99%

Long intergenic non-protein coding RNA 847 promotes laryngeal squamous cell carcinoma progression through the microRNA-181a-5p/zinc finger E-box binding homeobox 2 axis

XiaoLin

2022

Bioengineered

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“…In a recent study increased expression of NPM was reported in 82% of laryngeal cancer tissues and NPM knockdown inhibited laryngeal cancer cell survival [23]. The full results revealed an oncogenic role for NPM in laryngeal cancer through its effects on apoptosis and cellular growth.…”

Section: Discussionmentioning

confidence: 92%

“…Parallel in vitro studies revealed that vitamin D treatment of HNC cell lines significantly altered miRs regulating genes involved in many cancer pathways (i.e., steroid biosynthesis, cell proliferation, angiogenesis, chemokine, stem cell pluripotency, MAPK, and WNT signaling). Similarly, proteomic profiling following vitamin D treatment revealed modulation of proteins with roles in HNC cancer progression, metastasis, chemoresistance, and cancer recurrence and further supporting a potential role vitamin D in targeted cancer prevention [20][21][22][23].…”

Section: Introductionmentioning

confidence: 80%

“…Nucleophosmin (NPM), is associated with evasion of apoptosis, increased cancer cell viability, growth, and cell proliferation [ 105 ], and was down-regulated following vitamin D treatment of SCC-25 cells. In a recent study increased expression of NPM was reported in 82% of laryngeal cancer tissues and NPM knockdown inhibited laryngeal cancer cell survival [ 23 ]. The full results revealed an oncogenic role for NPM in laryngeal cancer through its effects on apoptosis and cellular growth.…”

Section: Discussionmentioning

confidence: 99%

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Disparities in Head and Neck Cancer: A Case for Chemoprevention with Vitamin D

et al. 2020

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Blacks experience disproportionate head and neck cancer (HNC) recurrence and mortality compared to Whites. Overall, vitamin D status is inversely associated to HNC pointing to a potential protective linkage. Although hypovitaminosis D in Blacks is well documented it has not been investigated in Black HNC patients. Thus, we conducted a prospective pilot study accessing vitamin D status in newly diagnosed HNC patients stratified by race and conducted in vitro studies to investigate mechanisms associated with potential cancer inhibitory effects of vitamin D. Outcome measures included circulating levels of vitamin D, related nutrients, and risk factor characterization as well as dietary and supplemental estimates. Vitamin D-based in vitro assays utilized proteome and microRNA (miR) profiling. Nineteen patients were enrolled, mean circulating vitamin D levels were significantly reduced in Black compared to White HNC patients, 27.3 and 20.0 ng/mL, respectively. Whites also supplemented vitamin D more frequently than Blacks who had non-significantly higher vitamin D from dietary sources. Vitamin D treatment of HNC cell lines revealed five significantly altered miRs regulating genes targeting multiple pathways in cancer based on enrichment analysis (i.e., negative regulation of cell proliferation, angiogenesis, chemokine, MAPK, and WNT signaling). Vitamin D further altered proteins involved in cancer progression, metastasis and survival supporting a potential role for vitamin D in targeted cancer prevention.

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“…In our ceRNA network, we found that 20 circRNAs and 26 mRNAs had a total of 10 miRNA binding sites, which were obviously related to apoptosis and inflammation. MAX, an important apoptosis gene, was upregulated by direct binding to the miR-181a promoter to increase MYCT1 expression, leading to apoptosis ( 59 ). In our study, we found that miR-2305 was able to regulate MAX and BCL2 in both ceRNA networks, and multiple circRNAs had binding sites with miR-2305 ( 60 ).…”

Section: Discussionmentioning

confidence: 99%

N6-Methyladenosine-Modified circRNA in the Bovine Mammary Epithelial Cells Injured by Staphylococcus aureus and Escherichia coli

Lin

Li³

et al. 2022

Front. Immunol.

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Mastitis is a common disease that hinders the development of dairy industry and animal husbandry. It leads to the abuse of antibiotics and the emergence of super drug-resistant bacteria, and poses a great threat to human food health and safety. Staphylococcus aureus (S. aureus) and Escherichia coli (E. coli) are the most common pathogens of mastitis in dairy cows and usually cause subclinical or clinical mastitis. CircRNAs and N6-methyladenosine (m6A) play important roles in immunological diseases. However, the mechanisms by which m6A modifies circRNA in bovine mammary epithelial cells remain poorly understood. The aim of our study was to investigate m6A-modified circRNAs in bovine mammary epithelial cells (MAC-T cells) injured by S. aureus and E. coli. The profile of m6A-modified circRNA showed a total of 1,599 m6A peaks within 1,035 circRNAs in the control group, 35 peaks within 32 circRNAs in the S. aureus group, and 1,016 peaks within 728 circRNAs in the E. coli group. Compared with the control group, 67 peaks within 63 circRNAs were significantly different in the S. aureus group, and 192 peaks within 137 circRNAs were significantly different in the E. coli group. Furthermore, we found the source genes of these differentially m6A-modified circRNAs in the S. aureus and E. coli groups with similar functions according to GO and KEGG analyses, which were mainly associated with cell injury, such as inflammation, apoptosis, and autophagy. CircRNA–miRNA–mRNA interaction networks predicted the potential circRNA regulation mechanism in S. aureus- and E. coli-induced cell injury. We found that the mRNAs in the networks, such as BCL2, MIF, and TNFAIP8L2, greatly participated in the MAPK, WNT, and inflammation pathways. This is the first report on m6A-modified circRNA regulation of cells under S. aureus and E. coli treatment, and sheds new light on potential mechanisms and targets from the perspective of epigenetic modification in mastitis and other inflammatory diseases.

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MYCT1 represses apoptosis of laryngeal cancerous cells through the MAX/miR‐181a/NPM1 pathway

Cited by 22 publications

References 45 publications

Long intergenic non-protein coding RNA 847 promotes laryngeal squamous cell carcinoma progression through the microRNA-181a-5p/zinc finger E-box binding homeobox 2 axis

Long intergenic non-protein coding RNA 847 promotes laryngeal squamous cell carcinoma progression through the microRNA-181a-5p/zinc finger E-box binding homeobox 2 axis

Disparities in Head and Neck Cancer: A Case for Chemoprevention with Vitamin D

N6-Methyladenosine-Modified circRNA in the Bovine Mammary Epithelial Cells Injured by Staphylococcus aureus and Escherichia coli

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