From predator to protector: Myxococcus fulvus WCH05 emerges as a potent biocontrol agent for fire blight.

Fire blight, caused by the Gram-negative bacterium Erwinia amylovora, poses a substantial threat to pome fruit production worldwide. Despite existing control strategies, a pressing need remains for sustainable and environmentally friendly fire blight management. Myxobacteria, renowned for their predatory behavior and potent enzymes, emerge as a groundbreaking biocontrol approach with significant potential. Here, we report the biocontrol potential of a novel Myxococcus fulvus WCH05, against E. amylovora. Using various in vitro and planta assays, we demonstrated the multifaceted biocontrol abilities of strain WCH05. In plate predation assays, strain WCH05 exhibited not only strong predation against E. amylovora but also broad-spectrum activities against other plant pathogenic bacteria. Pre-treatment with strain WCH05 significantly decreased pear blossom blight incidence in detached inflorescence assays, achieving a controlled efficacy of 76.02% that rivaled the antibiotic streptomycin (79.79%). In greenhouse trials, strain WCH05 effectively reduced the wilting rate and disease index in young pear seedlings, exhibiting both protective (73.68%) and curative (68.66%) control. Further investigation revealed that the biocontrol activity of strain WCH05 relies on both direct contact and extracellular enzyme secretion. While cell extracts lacked inhibitory activity, ammonium sulfate-precipitated secreted proteins displayed potent lytic activity against E. amylovora. Substrate spectrum analysis identified peptidases, lipases, and glycosidases among the secreted enzymes, suggesting their potential roles in pathogen degradation and biocontrol efficacy. This study presents the first evidence of Myxococcus fulvus WCH05 as a biocontrol agent against fire blight. Its potent predatory abilities and enzymatic arsenal highlight its potential for sustainable disease management in pome fruit production. Future research will focus on identifying and characterizing specific lytic enzymes and optimizing strain WCH05 application strategies for field efficacy.

Exploring potential correlations between bacterial communities, organic acids, and volatile metabolites of traditional fermented sauerkraut collected from different regions of Heilongjiang Province in Northeast China.

In this study, the bacterial communities and flavor metabolites of 27 traditional naturally fermented sauerkraut samples collected from nine regions of Heilongjiang Province in Northeast China were investigated. The dominant genera were Lactobacillus, Pseudomonas, Alcaligenes, Arcobacter, Pseudarcobacter, Lactococcus, Comamonas, Pediococcus, Prevotella, and Insolitispirillum. A total of 148 volatile compounds were detected in seven categories; esters and acids were the most abundant volatiles. Additionally, the highest content (15.96 mg/g) of lactic acid was detected in YC1. Acetic acid, oleic acid, palmitic acid, elaidic acid, and dehydroacetic acid were the key differential volatile compounds, which may be related to the bacterial communities. Spearman's correlation analysis revealed that Lactococcus and Lactobacillus were significantly positively correlated with flavor metabolites, suggesting that they may play a more significant role in flavor formation. The results of this study can help in the development of better quality of fermented vegetables.

Combination of ultrasound treatment and starter culture for improving the quality of beef jerky.

The effects of treatment by ultrasound (US), inoculation of Pediococcus acidilactici BP2 strain (BP), and their combination (US-BP) on the quality characteristics of beef jerky were investigated during fermentation for 6 days. Moisture contents and water activity were highest after the US and US-BP treatments (P < 0.05). These effects were attributed to the decreased moisture mobility in beef jerky during ultrasonication. Meanwhile, samples treated with US and US-BP displayed more broken muscle fibers and larger gaps and cavities between the adjacent muscle bundles, resulting in lower shear force values compared to the other samples (P < 0.05), which indicated that the US and US-BP treatments improved the tenderness of beef jerky. Moreover, treatment with BP promoted the flavor development of beef jerky. The US-BP treatment improved the sensory attributes of beef jerky. In conclusion, US-BP is a promising strategy to improve the quality of beef jerky.

Methylation Mediated Downregulation of TOB1-AS1 and TOB1 Correlates with Malignant Progression and Poor Prognosis of Esophageal Squamous Cell Carcinoma.

BACKGROUND: TOB1, a member of the transducer of erbB-2 /B-cell translocation gene family, was detected to be down-regulated in ESCC by RNA sequencing. TOB1-AS1, a head-to-head antisense lncRNA with TOB1, was down-regulated in several cancers. However, the roles of them in esophageal squamous cell carcinoma (ESCC) remained unclarified. AIMS: To investigate the roles and functions of TOB1-AS1 and TOB1 in ESCC tumorigenesis. MATERIALS AND METHODS: The expression levels, methylation status, biological function and mechanisms of TOB1-AS1 and TOB1 in ESCC were, respectively, detected. RESULTS: Frequent down-regulation of TOB1-AS1 and TOB1 was verified in esophageal cancer cells and ESCC tissues, and there was a positive correlation between them in ESCC tissues. The CpG sites hypermethylation within proximal promoter of TOB1-AS1 and TOB1 could lead to transcriptional inhibition of both genes. Furthermore, expression and proximal promoter methylation status of TOB1-AS1 or TOB1 may be associated with ESCC patients' prognosis. TOB1-AS1 and TOB1 may function as tumor suppressors by inhibiting growth, migration, and invasion of esophageal cancer cells. Up-regulation of TOB1-AS1 increased expression level of TOB1, and TOB1-AS1 could work as a ceRNA to modulate ATF3 expression via competitively binding with miR-103a-2-5p. Meanwhile, ATF3, as a transcription factor, could regulate transcription of TOB1; down-regulation of TOB1-AS1 in ESCC led to decreased expression of ATF3 through ceRNA mechanism, and further influenced the transcription of TOB1. CONCLUSION: TOB1-AS1 and TOB1 may act as tumor suppressors and may serve as potential targets for antitumor therapy in ESCC.

KTN1-AS1, a SOX2-mediated lncRNA, activates epithelial-mesenchymal transition process in esophageal squamous cell carcinoma.

Kinectin 1 antisense RNA 1 (KTN1-AS1), a long non-coding RNA (lncRNA), has been proved to have tumor-promoting properties and its expression is enhanced in several human tumors. However, the role of KTN1-AS1 in the pathogenesis of esophageal squamous cell carcinoma (ESCC) remains unknown. This study aimed to investigate the expression status, functional roles, and molecular mechanisms of KTN1-AS1 in the development of ESCC. Considerable upregulation of KTN1-AS1 was confirmed in esophageal cancer cells and ESCC tissues and its expression was associated with TNM stage, pathological differentiation, and lymph node metastasis. SOX2 directly activated transcription of KTN1-AS1, and overexpression of KTN1-AS1 facilitated ESCC cells proliferation and invasion in vitro and in vivo. Furthermore, KTN1-AS1 could bind to retinoblastoma binding protein 4 (RBBP4) in the nucleus and enhanced its binding with histone deacetylase 1 (HDAC1), thereby activating the epithelial-mesenchymal transition (EMT) process through downregulating E-cadherin expression at the epigenetic level. In conclusion, KTN1-AS1, induced by SOX2, acts as a tumor-promoting gene and may serve as a potential therapeutic and prognostic biomarker for ESCC.

Antisense lncRNA PCNA-AS1 promotes esophageal squamous cell carcinoma progression through the miR-2467-3p/PCNA axis.

Multiple studies have indicated that long non-coding RNAs are aberrantly expressed in cancers and are pivotal in developing various tumors. No studies have investigated the expression and function of long non-coding antisense RNA PCNA-AS1 in esophageal squamous cell carcinoma (ESCC). In this study, the expression of PCNA-AS1 was identified by qRT-PCR. Cell function assays were used to explore the potential effect of PCNA-AS1 on ESCC progression. A prediction website was utilized to discover the relationships among PCNA-AS1, miR-2467-3p and proliferating cell nuclear antigen (PCNA). Dual luciferase reporter gene and RNA immunoprecipitation (RIP) assays were executed to verify the binding activity between PCNA-AS1, miR-2467-3p and PCNA. As a result, PCNA-AS1 was highly expressed in ESCC and was associated with patient prognosis. PCNA-AS1 overexpression strongly contributed to ESCC cell proliferation, invasion and migration. PCNA-AS1 and PCNA were positively correlated in ESCC. Bioinformatics analysis, RIP and luciferase reporter gene assays revealed that PCNA-AS1 could act as a competitive endogenous RNA to sponge miR-2467-3p, thus upregulating PCNA. In conclusion, the current outcome demonstrates that PCNA-AS1 may be a star molecule in the treatment of ESCC.

Corrigendum: LncRNA FOXP4-AS1 promotes the progression of esophageal squamous cell carcinoma by interacting with MLL2/H3K4me3 to upregulate FOXP4.

[This corrects the article DOI: 10.3389/fonc.2021.773864.].

E2F1-activated NRSN2 promotes esophageal squamous cell carcinoma progression through AKT/mTOR pathway.

BACKGROUND: Neurensin­2 (NRSN2) has been reported to act as an oncogene in several types of human cancer. However, the molecular mechanism of NRSN2 in esophageal squamous cell carcinoma (ESCC) remains to be elucidated. METHODS: The mRNA expression levels of NRSN2 in ESCC tissues and cell lines were evaluated by quantitative real-time PCR (qRT-PCR). The protein expression levels of NRSN2 in ESCC tissues were measured by Immunohistochemical (IHC) method. Luciferase reporter and chromatin immunoprecipitation assays were conducted to confirm the upstream transcription factor of NRSN2. Loss- and gain-function assays were conducted to evaluate the effects of NRSN2 on ESCC cells proliferation, migration, and invasion. The function of NRSN2 was validated in vivo using tumor xenografts. The relationship between NRSN2 and AKT/mTOR pathway were confirmed by western blot assay. RESULTS: The expression level of NRSN2 was increased in ESCC tissues and cell lines. High expression level of NRSN2 was correlated with depth of invasion, lymph node metastasis, TNM stage, and poor prognosis of ESCC patients. NRSN2 was transcribed by E2F1. Knockdown of NRSN2 significantly inhibited ESCC cells proliferation, migration, and invasion, whereas NRSN2 overexpression showed reverse phenotypes. Overexpression of NRSN2 also enhanced ESCC tumorigenicity in vivo. Furthermore, the E2F1/NRSN2 axis promoted proliferation, migration, and invasion of ESCC cells by activating the AKT/mTOR pathway. CONCLUSION: NRSN2 is a direct transcriptional target of E2F1 to promote tumor progression in ESCC. NRSN2 may be a diagnostic biomarker or treatment target for ESCC.

Long noncoding RNA TFAP2A-AS1 promotes oral squamous cell carcinoma cell growth and movement via competitively binding miR-1297 and regulating TFAP2A expression.

Oral squamous cell carcinoma (OSCC) is an aggressive and common malignancy in the head and neck, characterized by poor prognosis and high incidence. This study aimed to investigate the role of long noncoding RNA TFAP2A-AS1 in OSCC. The competing endogenous RNA network of TFAP2A-AS1 was constructed by bioinformatics analysis. The expressions of miR-1297, TFAP2A-AS1, and TFAP2A were measured by quantitative reverse transcription-polymerase chain reaction. The correlations of TFAP2A-AS1, miR-1297, and TFAP2A with clinicopathological characteristics of OSCC were assessed. RNA immunoprecipitation and dual-luciferase reporter assay were used to identify the target of miR-1297. Cell proliferation was measured by colony formation assay and [3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium] assay. Transwell assay and wound healing assay were performed to assess cell movement. TFAP2A-AS1 and TFAP2A were upregulated in OSCC and their expression levels were positively correlated. The levels of TFAP2A-AS1, miR-1297, and TFAP2A were also associated with lymphatic metastasis and the tumor-node-metastasis (TNM) stage of OSCC patients. TFAP2A-AS1 acted as a miR-1297 sponge. OSCC cell growth and movement were inhibited by miR-1297. Changes in the miR-1297 expression abolished the effects of TFAP2A-AS1 on OSCC cells. Additionally, TFAP2A was a target of miR-1297. TFAP2A promoted OSCC cell growth and migration/invasion, indicating that TFAP2A mediated the effects of TFAP2A-AS1 and miR-1297. TFAP2A-AS1 exerts an oncogenic effect in OSCC via the TFAP2A-AS1/miR-1297/TFAP2A axis, which may provide new targets and strategies for OSCC treatments.

Long non-coding RNA NRSN2-AS1, transcribed by SOX2, promotes progression of esophageal squamous cell carcinoma by regulating the ubiquitin-degradation of PGK1.

Aberrant expression of long non-coding RNAs (lncRNAs) plays pivotal roles in tumorigenesis of human malignant cancers, including esophageal squamous cell carcinoma (ESCC). However, the specific role of lncRNA NRSN2-AS1 in ESCC has not been investigated. Our analysis of clinical data revealed that NRSN2-AS1 was upregulated in ESCC tissues and negatively correlated with patient survival. Luciferase reporter assays and chromatin immunoprecipitation assays demonstrated that NRSN2-AS1 is transcribed by SOX2. In vitro functional experiments showed that NRSN2-AS1 can promote ESCC cell proliferation, migration, and invasion. Furthermore, NRSN2-AS1-binding proteins were detected using RNA pull-down assays and mass spectrometry. Mechanistically, NRSN2-AS1 can bind to phosphoglycerate kinase 1 (PGK1) and upregulate its protein levels by inhibiting its ubiquitination. Knockdown of PGK1 in part abolished the NRSN2-AS1 overexpression-induced effects on ESCC cell proliferation, migration, invasion, and epithelial­mesenchymal transition (EMT). Thus, NRSN2-AS1 may be a diagnostic biomarker or treatment target for ESCC.

Downregulation of LINC00886 facilitates epithelial-mesenchymal transition through SIRT7/ELF3/miR-144 pathway in esophageal squamous cell carcinoma.

LINC00886 has been reported to be down-regulated in laryngeal squamous cell carcinoma, and aberrant DNA methylation status of it has been screened in several tumor types. However, the roles of LINC00886 in esophageal squamous cell carcinoma (ESCC) remained unclarified. The present study was to investigate the expression level, epigenetic inactivation mechanisms, and functions of LINC00886 in ESCC tumorigenesis. Frequent down-regulation of LINC00886 was verified in esophageal cancer cells and ESCC tissues. There are CpG islands spanning the promoter and exon 1 regions of LINC00886 gene, and DNA hypermethylation of proximal promoter led to transcriptional inhibition of LINC00886, moreover, histone modification also played certain roles in LINC00886 transcription. LINC00886 functioned as a tumor suppressor by inhibiting proliferation, migration, and invasion of esophageal cancer cells. LINC00886 was down-regulated following TGF-ß1 treatment in esophageal cancer cells and participated in epithelial-mesenchymal transition (EMT) process by regulating EMT-related genes, especially ZEB1 and ZEB2. ELF3 was proved to be one of the downstream target genes of LINC00886. LINC00886 may interact with and recruit SIRT7 to decrease acetylation level of H3K18 on the promoter region of ELF3 to inhibit its expression. Furthermore, ELF3 may promote EMT process via promoting ZEB1 and ZEB2 expression through binding to the promoter region of miR-144 to suppress miR-144-3p transcriptional activity in ESCC. These data suggest that LINC00886 may act as a tumor suppressor gene in ESCC and its down-regulation through epigenetic mechanisms promotes EMT process via SIRT7/ELF3/miR-144 pathway in ESCC. Thus, LINC00886 may be a potential therapeutic target for ESCC treatment.

LncRNA GATA2-AS1 suppresses esophageal squamous cell carcinoma progression via the mir-940/PTPN12 axis.

Esophageal squamous cell carcinoma (ESCC) is a common malignant tumor worldwide. Long noncoding RNAs (lncRNAs) exhibit a regulatory role in the progression of ESCC. Our research was performed to investigate the potential molecular mechanism of lncRNA GATA2-AS1 in ESCC. METHODS: The expression of GATA2-AS1 was identified by qRT-PCR. Cell function assays explored the potential effect of GATA2-AS1 on ESCC progression. The subcellular hierarchical localization method was executed to identify the subcellular localization of GATA2-AS1 in ESCC cells. A prediction website was utilized to discover the relationships among GATA2-AS1, miR-940 and PTPN12. Dual luciferase reporter gene, pull-down assays and RIP assays were executed to verify the binding activity among GATA2-AS1, miR-940 and PTPN12. Xenograft tumor experiments were performed to evaluate ESCC cell growth in vivo. RESULTS: The expression of GATA2-AS1 and PTPN12 was reduced, while miR-940 expression was enhanced in ESCC tissues and cell lines. In vivo experiments showed that GATA2-AS1 inhibited the progression of ESCC cells toward malignancy. Bioinformatics analysis, dual luciferase and RIP assays revealed that GATA2-AS1 upregulated PTPN12 expression by competitively targeting miR-940. miR-940 reversed the inhibitory effect of GATA2-AS1 on the biological behavior of ESCC cells. CONCLUSION: Our findings suggested that GATA2-AS1, expressed at low levels in ESCC, plays a crucial role in the progression of ESCC by targeting the miR-940/PTPN12 axis and could be a potential drug target to treat ESCC patients.

Computer vision to recognize construction waste compositions: A novel boundary-aware transformer (BAT) model.

Recognition of construction waste compositions using computer vision (CV) is increasingly explored to enable its subsequent management, e.g., determining chargeable levy at disposal facilities or waste sorting using robot arms. However, the applicability of existing CV-enabled construction waste recognition in real-life scenarios is limited by their relatively low accuracy, characterized by a failure to distinguish boundaries among different waste materials. This paper aims to propose a novel boundary-aware Transformer (BAT) model for fine-grained composition recognition of construction waste mixtures. First, a pre-processing workflow is devised to separate the hard-to-recognize edges from the background. Second, a Transformer structure with a self-designed cascade decoder is developed to segment different waste materials from construction waste mixtures. Finally, a learning-enabled edge refinement scheme is used to fine-tune the ignored boundaries, further boosting the segmentation precision. The performance of the BAT model was evaluated on a benchmark dataset comprising nine types of materials in a cluttered and mixture state. It recorded a 5.48% improvement of MIoU (mean intersection over union) and 3.65% of MAcc (Mean Accuracy) against the baseline. The research contributes to the body of interdisciplinary knowledge by presenting a novel deep learning model for construction waste material semantic segmentation. It can also expedite the applications of CV in construction waste management to achieve a circular economy.

SNHG17, as an EMT-related lncRNA, promotes the expression of c-Myc by binding to c-Jun in esophageal squamous cell carcinoma.

Dysregulation of long noncoding RNA SNHG17 is associated with the occurrence of several tumors; however, its role in esophageal squamous cell carcinoma (ESCC) remains obscure. The present study demonstrated that SNHG17 was upregulated in ESCC tissues and cell lines, induced by TGF-ß1, and associated with poor survival. It is also involved in the epithelial-to-mesenchymal transition (EMT) process. The mechanism underlying SNHG17-regulated c-Myc was detected by RNA immunoprecipitation, RNA pull-down, chromatin immunoprecipitation, and luciferase reporter assays. SNHG17 was found to directly regulate c-Myc transcription by binding to c-Jun protein and recruiting the complex to specific sequences of the c-Myc promoter region, thereby increasing its expression. Moreover, SNHG17 hyperactivation induced by TGF-ß1 results in PI3K/AKT pathway activation, promoting cells EMT, forming a positive feedback loop. Furthermore, SNHG17 facilitated ESCC tumor growth in vivo. Overall, this study demonstrated that the SNHG17/c-Jun/c-Myc axis aggravates ESCC progression and EMT induction by TGF-ß1 and may serve as a new therapeutic target for ESCC.

LncRNA FOXP4-AS1 Promotes the Progression of Esophageal Squamous Cell Carcinoma by Interacting With MLL2/H3K4me3 to Upregulate FOXP4.

Malignant tumors are a grave threat to human health. Esophageal squamous cell carcinoma (ESCC) is a common gastrointestinal malignant tumor. China has a high incidence of ESCC, and its morbidity and mortality are higher than the global average. Increasingly, studies have shown that long noncoding RNAs (lncRNAs) play a vital function in the occurrence and development of tumors. Although the biological function of FOXP4-AS1 has been demonstrated in various tumors, the potential molecular mechanism of FOXP4-AS1 in ESCC is still poorly understood. The expression of FOXP4 and FOXP4-AS1 was detected in ESCC by quantitative real-time PCR (qRT-PCR) or SP immunohistochemistry (IHC). shRNA was used to silence gene expression. Apoptosis, cell cycle, MTS, colony formation, invasion and migration assays were employed to explore the biological functions of FOXP4 and FOXP4-AS1. The potential molecular mechanism of FOXP4-AS1 in ESCC was determined by dual-luciferase reporter, RNA immunoprecipitation (RIP) and chromatin immunoprecipitation (ChIP). Here, we demonstrated that FOXP4-AS1 was significantly increased in ESCC tissues and cell lines, associated with lymph node metastasis and TNM staging. Cell function experiments showed that FOXP4-AS1 promoted the proliferation, invasion and migration ability of ESCC cells. The expression of FOXP4-AS1 and FOXP4 in ESCC tissues was positively correlated. Further research found that FOXP4-AS1, upregulated in ESCC, promotes FOXP4 expression by enriching MLL2 and H3K4me3 in the FOXP4 promoter through a "molecular scaffold". Moreover, FOXP4, a transcription factor of ß-catenin, promotes the transcription of ß-catenin and ultimately leads to the malignant progression of ESCC. Finally, FOXP4-AS1 may be a new therapeutic target for ESCC.

LncRNA DDX11 antisense RNA 1 promotes EMT process of esophageal squamous cell carcinoma by sponging miR-30d-5p to regulate SNAI1/ZEB2 expression and Wnt/ß-catenin pathway.

LncRNA DDX11 antisense RNA 1 (DDX11-AS1) is recognized as having an imperative oncogenic role in different types of human cancer. Nevertheless, the functions, as well as the basic mechanisms of DDX11-AS1 in the EMT process of esophageal squamous cell carcinoma (ESCC), are yet to be clarified. In this research, high DDX11-AS1 expression was detected in ESCC cells as well as tissues and was linked to the poor prognosis of patients with ESCC. DDX11-AS1 promoted cell proliferation, migration, invasion ability and epithelial mesenchymal transition (EMT) process in vitro. Mechanistic analysis depicted that DDX11-AS1 may function as a ceRNA through sponging miR-30d-5p to upregulate the expression of SNAI1 and ZEB2. Meanwhile, overexpression of DDX11-AS1 might cause the activation of the Wnt/ß-catenin signaling pathway via targeting miR-30d-5p. On the whole, the findings of this research illustrate that DDX11-AS1 may act as an EMT-related lncRNA to advance ESCC progression through sponging miR-30d-5p to regulate SNAI1/ZEB2 expression and activate the Wnt/ß-catenin pathway, which indicates that it might serve as a probable therapeutic target for ESCC.

FOXD3 suppresses epithelial-mesenchymal transition through direct transcriptional promotion of SMAD7 in esophageal squamous cell carcinoma.

The transcription factor forkhead box D3 (FOXD3) is an important member of the FOX family, which can maintain the pluripotent properties of cell clusters, neural crest, and trophoblastic progenitor cells in vivo. It has been shown that FOXD3 could affect proliferation, migration, and angiogenesis of various tumors and its deletion and overexpression in organisms will undoubtedly have important influence on the change of cell fate and the occurrence of tumors. However, the underlying functions and molecular mechanisms of FOXD3 in esophageal squamous cell carcinoma (ESCC) have not been fully clarified. According to the present study, the expression levels and functional roles of FOXD3 were investigated, and its prognostic value and molecular mechanisms in tumorigenesis and progression of ESCC were clarified. The expression level of FOXD3 was significantly downregulated in ESCC tissues and cell lines, and correlated with gender, family history of upper gastrointestinal cancer, TNM stage, depth of invasion, lymph node metastasis, and ESCC patients' survival. Moreover, FOXD3 inhibited cells migration and invasion as well as participated in TGF-ß1 induced epithelial-mesenchymal transition process. Furthermore, a positive correlation between FOXD3 and SMAD family member 7 (SMAD7) was explored in ESCC. FOXD3 could directly bind to promoter regions of SMAD7 gene, leading to transcriptional promotion of SMAD7 in human esophageal cancer cells. Taken together, FOXD3 may play a tumor suppressor role in ESCC and may be applied as a new therapeutic target and prognostic marker for ESCC.

IncRNA ZNF667-AS1 Suppresses Epithelial Mesenchymal Transformation by Targeting TGF-ß1 in Oral Squamous Cell Carcinoma.

BACKGROUND: IncRNAs perform complex functions and play an essential role in all stages of tumor progression. However, there are few studies that discuss the function of lncRNA ZNF667-AS1in oral squamous cell carcinoma (OSCC). This study aimed at analyzing the expression and biological behavior of lncRNA ZNF667-AS1 in OSCC. METHODS: IncRNA ZNF667-AS1 expression level in OSCC tissues and cell lines was explored by real-time PCR. The role of lncRNA ZNF667-AS1 on prognosis was elucidated. Cell proliferation assay, plate colony formation assay, wound-healing assay, and transwell migration assay were used to detect cell proliferation ability, cell clone formation ability, migration ability, and invasion ability, respectively. The effect of lncRNA ZNF667-AS1 on epithelial mesenchymal transformation (EMT) process was evaluated by western blot and real-time PCR. RESULTS: The expression levels of lncRNA ZNF667-AS1 were decreased in malignant tumor tissues. The OSCC patients with high expression of lncRNA ZNF667-AS1 had a longer survival time. IncRNA ZNF667-AS1 inhibited cell proliferation, cell clone formation ability, invasion and migration. Furthermore, lncRNA ZNF667-AS1 could inhibit the EMT process by suppressing transforming growth factor-ß-1 (TGF-ß1) expression, and TGF-ß1 treatment could partially restore the inhibitory effect. CONCLUSIONS: IncRNA ZNF667-AS1 may act as an antioncogene inhibiting the ability of proliferation, cell clone formation, invasion and migration, and suppress the process of EMT by targeting TGF-ß1. IncRNA ZNF667-AS1 could be a potential therapeutic target and a new predictive biological marker of OSCC.

LINC00239 Interacts with C-Myc Promoter-Binding Protein-1 (MBP-1) to Promote Expression of C-Myc in Esophageal Squamous Cell Carcinoma.

Increasing evidence demonstrates that long non-coding RNAs (lncRNA) play a vital role in the progression of tumors, containing esophageal squamous cell carcinoma (ESCC). LINC00239 was reported as an oncogene in diverse kinds of cancers, whereas its specific role is still unclear in ESCC. In this study, we detected the expression and functional role of LINC00239 in ESCC specimens and cells, and investigated the molecular mechanisms of it. LINC00239 was highly expressed in ESCC tissues and cells, and was related to poor prognosis of patients with ESCC. The proliferation, metastasis, and invasion ability as well as epithelial-mesenchymal transition (EMT) process were all enhanced in LINC00239-overexpressed ESCC cells. LINC00239 was upregulated in TGF-ß1-treated ESCC cells. Furthermore, LINC00239 was found to bind directly to the transcription factor c-Myc promoter-binding protein-1 (MBP-1). MBP-1 was detected to inhibit the transcription of c-Myc in ESCC. Moreover, LINC00239 could activate c-Myc transcription through influencing MBP-1-binding ability to c-Myc promoter. These data suggest that LINC00239 may act as an oncogene to promote the transcription of c-Myc by competitively combining with MBP-1 in ESCC, and may serve as a potential target for antitumor therapy in ESCC. IMPLICATIONS: LINC00239 may function as an oncogenic lncRNA in ESCC through the LINC00239/MBP-1/c-Myc axis to activate EMT process.

MicroRNA-27a promotes tumorigenesis in tongue squamous cell carcinoma by enhancing proliferation, migration and suppressing apoptosis.

BACKGROUND: Tongue squamous cell carcinoma (TSCC) is a major subtype of head and neck squamous cell carcinoma (HNSCC), which is an intractable cancer with a poor prognosis. Studies have shown that microRNAs (miRNAs) play an important role in TSCC biology. However, the expression and functions of miRNAs in TSCC remain unclear. METHODS: The non-coding RNA profiles of TSCC were downloaded from the GEO database. WGCNA (Weighted gene co-expression network analysis) and differential expression miRNA (DE-miRNA) analyses were employed to identify key candidate miRNAs. miRNA expression was detected using RT-qPCR analysis. The target genes of key miRNAs were predicted. Gene ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were performed to explore the potential functions and pathways of key miRNA. miRNA inhibitor was transfected to detect the function of miRNA. The effect of miRNA deregulation on TSCC cell proliferation and apoptosis was investigated using MTS, Annexin V-FITC/PI double staining, and flow cytometry assays. RESULTS: miR-27a was a key miRNA in TSCC, which was significantly up-regulated in both Cal-27 cells and malignant tissues from the TSCC patients. In addition, functional analysis showed that miR-27a was involved in the regulation of the MAPK, ERBB, and Jak-STAT signaling pathways. Moreover, RHOA and PRKACA were potential target genes of miR-27a, suggesting them as possible mediators of the tumor-promoting effect of miR-27a. Moreover, downregulation of miR-27a inhibited cell proliferation and facilitated cell apoptosis in Cal-27 cells. CONCLUSION: Our findings strongly suggest that miR-27a could promote the tumorigenesis and development of TSCC, which makes it a potential new diagnostic marker and therapeutic target for TSCC.