Blomleblanc4778

ACC is extremely rare; it is difficult to observe a specific genetic pattern and NGS can provide a lot of information about the genetic causes of this disease. Our work shows that the MET p.Thr1010Ile mutation can be associated with the hereditary occurrence of ACC.

The current study was designed to investigate the functionality of lncRNA CCHE1 in nasopharyngeal carcinoma.

MiRNA levels of lncRNA CCHE1 were examined by RT-qPCR. CCK8 assay and colony formation assay were together performed to detect cell proliferation viability. Furthermore, wound healing assay and transwell assay were respectively conducted to assess cell migration and invasion. In addition, proteins related to MEK/ERK/c-MYC pathway were detected by Western blot.

Elevated levels of CCHE1 were verified in NPC cell lines. Downregulation of CCHE1 significantly inhibited tumor growth and suppressed A549 cell proliferation, migration and invasion. MEK/ERK/c-MYC pathway was activated in nasopharyngeal carcinoma. Treatment of PD98059 (MEK inhibitor) or SCH772984 (ERK inhibitor) reversed the effects of CCHE1 on cell proliferation, migration and invasion in NPC.

The present study suggested that downregulation of lncRNA CCHE1 could inhibit cell proliferation, migration and invasion by suppressing MEK/ERK/c-MYC pathway in nasopharyngeal carcinoma.

The present study suggested that downregulation of lncRNA CCHE1 could inhibit cell proliferation, migration and invasion by suppressing MEK/ERK/c-MYC pathway in nasopharyngeal carcinoma.

The purpose of this study was to investigate GOLPH3 expression in nasopharyngeal carcinoma (NPC) and its influence on the metastatic ability of NPC cells; meanwhile, the underlying mechanism of GOLPH3 promoting the malignant progression of NPC was also explored.

In this study, quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to examine the expression of GOLPH3 in 34 pairs of tumor tissue and paracancerous tissue specimens collected from NPC patients, and the interplay between GOLPH3 expression and clinical indicators was analyzed, as well as the prognosis of NPC patients. Meanwhile, GOLPH3 expression in NPC cell lines was further verified by qRT-PCR assay. Furthermore, GOLPH3 knockdown model was constructed in NPC cell lines, including SUNE2 and CNE. Then, cell counting kit-8 (CCK-8), transwell invasion, and cell wound healing assays were applied to analyze the effect of GOLPH3 on the biological function of NPC cells. In addition, an in-depth study of the relationship between GOLPH is remarkably associated with lymph node metastasis and poor prognosis of NPC patients; in addition, it may promote the proliferation and metastatic ability of NPC cells by regulating E-cadherin.

The purpose of this study was to uncover the regulatory effect of LINC00887 on the progression of nasopharyngeal carcinoma (NPC) and the underlying mechanism.

Relative level of LINC00887 in NPC tissues and cells was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Thereafter, the regulatory effect of LINC00887 on proliferative ability in SUNE-1 and HK-1 cells was examined by cell counting kit-8 (CCK-8) and 5-Ethynyl-2'-deoxyuridine (EdU) assay. Through Dual-Luciferase reporter gene assay and RNA-Binding Protein Immunoprecipitation (RIP) assay, the interaction in the regulatory loop LINC00887/miRNA-203b-3p/NUP205 was ascertained. At last, rescue experiments were conducted to clarify the involvement of the regulatory loop LINC00887/miRNA-203b-3p/NUP205 in the progression of NPC.

Results showed that LINC00887 was upregulated in NPC tissues and cells, and its overexpression markedly stimulated the proliferative ability in NPC cells. click here In addition, a potential interaction in the regulatory loop LINC00887/miRNA-203b-3p/NUP205 was discovered, which was responsible for promoting the proliferative ability in NPC.

LINC00887 promotes the proliferative ability in NPC via absorbing miRNA-203b-3p to upregulate NUP205.

LINC00887 promotes the proliferative ability in NPC via absorbing miRNA-203b-3p to upregulate NUP205.

To explore the potential function of a candidate circular ribonucleic acid (circRNA) [human serum albumin (hsa)_circ_RNA0023397] in esophageal cancer cells.

Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was used to detect the expression level of hsa_circ_RNA0023397 in three esophageal cancer cell lines (KYSE-150, ECA109, and TE-1), which was compared with that in normal human esophageal epithelial cell line (HET-1A). The expression plasmid of hsa_circ_RNA0023397 was constructed, and the effect of overexpression of hsa_circ_RNA0023397 on cell proliferation was determined by cell counting kit-8 (CCK-8) and colony formation assay. The effect of overexpression of hsa_circ_RNA0023397 on cell apoptosis was detected by flow cytometry. Further bioinformatics analysis and Luciferase reporter gene analysis were carried out to explore the role of hsa_circ_RNA0023397 as a sponge of micro RNAs (miRNAs).

Compared with that in normal human esophageal epithelial cell line HET-1A, the expression of hsa_circ_RNA0023397 was down-regulated in three esophageal cancer cell lines in vitro. Overexpression of hsa_circ_RNA0023397 overtly inhibited KYSE-150 cell proliferation and promoted its apoptosis. Bioinformatics prediction and Luciferase reporter gene assay confirmed that hsa_circ_RNA0023397 could bind to miR-160b. MiR-106b participated in hsa_circ_RNA0023397-mediated inhibition of proliferation of esophageal cancer KYSE-150 cells.

Hsa_circ_RNA0023397 is down-regulated in esophageal cancer cells and can act as miR-106b to affect the biological function of esophageal cancer cells.

Hsa_circ_RNA0023397 is down-regulated in esophageal cancer cells and can act as miR-106b to affect the biological function of esophageal cancer cells.

The aim of this study is to investigate the expression levels of circRNA_100782 in gastric cancer tissues, and its function of regulating tumor suppressor gene Rb by absorbing miR-574-3p in a sponge form.

qRT-PCR was performed to detect the expressions of circRNA_100782 at different stages during gastric cancer tissues. CCK-8 assay was performed to evaluate the osteoclast proliferation and differentiation. The correlation between miR-574-3p and circRNA_100782 was detected by statistical analysis. Bioinformatics and Luciferase assay were performed to explore the interaction and binding site of circRNA_100782 and miR-574-3p. The mice Rb 3'-UTR were cloned into the Luciferase reporter vector and miR-574-3p binding mutants were constructed to validate the inhibited regulation of miR-574-3p to the expression of Rb.

In the current study, compared with adjacent non-cancerous normal tissues, the expressions of circRNA_100782 and Rb were both downregulated in human gastric cancer cells. Through qRT-PCR and CCK-8 assay, we found that the expression of circRNA_100782 is related to the proliferation of gastric cancer cells.