Gammelgaardniemann2037

It was discovered through the survival analysis that the expression of CCAT2 was notably associated with the poor prognosis of ATC patients. After knockdown of CCAT2, both the proliferation ability and the IC50 values of doxorubicin and cisplatin substantially declined in human thyroid carcinoma cells. The opposite conditions were found after CCAT2 was overexpressed in human thyroid carcinoma cells.

CCAT2 potentiates the proliferation ability and chemoresistance of cells, promotes the progression of thyroid carcinoma, and hinders the prognosis of ATC.

CCAT2 potentiates the proliferation ability and chemoresistance of cells, promotes the progression of thyroid carcinoma, and hinders the prognosis of ATC.

This study aims to uncover the differential expression of circRNA_100395 in breast carcinoma specimens, and its regulatory effect on cancer cell phenotypes. The role of circRNA_100395 in affecting breast carcinoma progression and the molecular mechanism are explored as well.

CircRNA_100395 expressions in breast carcinoma and paracancerous tissues were detected. The influence of circRNA_100395 level on clinical indicators of breast carcinoma patients was analyzed. In vitro regulations of circRNA_100395 on phenotypes of breast carcinoma cells were examined by CCK-8, colony formation, and transwell assay. The interaction between circRNA_100395 and MAPK6 was confirmed by Dual-Luciferase reporter assay and rescue assays.

CircRNA_100395 was downregulated in breast carcinoma tissues and cell lines. Its level was negatively correlated to tumor staging and tumor size of breast carcinoma. Overexpression of circRNA_100395 in SKBR3 and MDA-MB-231 cells weakened proliferative and migratory abilities. MAPK6 was the target gene of circRNA_100395. Overexpression of MAPK6 reversed the anti-cancer effect of circRNA_100395 on breast carcinoma.

CircRNA_100395 serves as an anti-cancer gene in breast carcinoma progression by targeting MAPK6, and its level is negatively correlated to tumor staging and tumor size of breast carcinoma. CircRNA_100395 can be utilized as a potential biomarker and therapeutic target of breast carcinoma.

CircRNA_100395 serves as an anti-cancer gene in breast carcinoma progression by targeting MAPK6, and its level is negatively correlated to tumor staging and tumor size of breast carcinoma. CircRNA_100395 can be utilized as a potential biomarker and therapeutic target of breast carcinoma.

Nasopharyngeal carcinoma (NPC) is one of the most ordinary head and neck tumors. This study aims to uncover the role of circ-ABCB10 functions in the progression of NPC.

The circ-ABCB10 expression was detected in paired NPC patients' tissue samples and cell lines. The role of circ-ABCB10 in NPC proliferation was identified through proliferation assay, Ethynyl deoxyuridine (EdU) assay and colony formation assay. Next, the role of circ-ABCB10 in NPC metastasis was measured through wound healing assay and transwell assay. Finally, the underlying mechanism was further uncovered through Western blot assay and real-time quantitative polymerase chain reaction (RT-qPCR).

It was found that circ-ABCB10 expression was significantly higher in NPC tissues than that in adjacent samples. In addition, cell proliferation, migration and invasion of NPC were promoted through overexpression of circ-ABCB10 in vitro. Results of further experiments revealed that ROCK1 was upregulated via overexpression of circ-ABCB10 in NPC.

This study indicated that circ-ABCB10 promoted NPC cell proliferation and metastasis via upregulating ROCK1 in vitro.

This study indicated that circ-ABCB10 promoted NPC cell proliferation and metastasis via upregulating ROCK1 in vitro.

To explore the roles of micro ribonucleic acid (miR)-199a-5p in the proliferation, apoptosis, invasion and metastasis of laryngeal cancer cells, and its molecular mechanisms.

The expression of miR-199a-5p in 25 cases of laryngeal cancer tissues and paracancerous tissues was detected via quantitative real-time polymerase chain reaction (qRT-PCR). Its expression in TU212, TU686 and human epithelial type 2 (HEp-2) laryngeal cancer cell lines and normal nasopharyngeal epithelial cell line NP69 was also detected via qRT-PCR. HEp-2 cells were transiently transfected with miR-199a-5p mimic or miR-199a-5p inhibitor, and the expression of miR-199a-5p was verified using RT-PCR after transfection. see more The regulatory effects of miR-199a-5p on the proliferation, apoptosis, invasion and migration abilities of HEp-2 cells were observed through methyl thiazolyl tetrazolium (MTT) assay, flow cytometry, wound healing assay and transwell assay, respectively. Then, the mechanisms of miR-199a-5p in regulating Caspase-3 activity arocess, whereas suppressing miR-199a-5p could accelerate the process.

The expression of miR-199a-5p in laryngeal cancer tissues is substantially lower than that in the paracancerous tissues. MiR-199a-5p suppresses proliferation, invasion and migration in laryngeal cancer cell proliferation, while triggers cell apoptosis.

The expression of miR-199a-5p in laryngeal cancer tissues is substantially lower than that in the paracancerous tissues. MiR-199a-5p suppresses proliferation, invasion and migration in laryngeal cancer cell proliferation, while triggers cell apoptosis.

To detect the expression pattern of raf-1 kinase inhibitor protein (RKIP) in oral squamous cell carcinoma (OSCC) samples and to explore its clinical significance in OSCC metastasis.

Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) and Western blot assay were conducted to detect the expression of RKIP in OSCC tissues and cells. The relationship between RKIP expression and OSCC clinicopathological characteristics was statistically analyzed. Transwell assay, wound healing assay, and Western blot were used to detect the influence of RKIP on the metastasis ability of OSCC cells.

RKIP was significantly downregulated in OSCC samples. Low expression of RKIP predicted high incidence of metastasis in OSCC patients. In vitro experiments demonstrated that overexpression of RKIP could significantly inhibit invasion and migration abilities of OSCC cells.

RKIP was a novel factor involved in OSCC progression, which was a potential biomarker and therapeutic target for the patients.

RKIP was a novel factor involved in OSCC progression, which was a potential biomarker and therapeutic target for the patients.