Laryngeal Primary Myoepithelial Carcinoma: Case Report and a Systematic Review of Literature.

Myoepithelial carcinoma of the head and neck is a rare malignant tumor that usually arises from the salivary glands but rarely from the larynx. Here, we describe 11 cases (one treated by us and 10 previously published) of laryngeal myoepithelial carcinoma. Our patient was a 60-year-old male who initially presented with hoarseness and throat pain. The patient had suffered from continuing hoarseness and throat pain for one month before he consulted an otorhinolaryngologist. Computed tomography (CT) scan showed a polypoid tumor involving the right vocal cords. Biopsy was performed, and the disease was pathologically diagnosed as myoepithelial carcinoma of the larynx by hematoxylin-eosin and immunohistochemical staining. The total follow-up period was 15 months. Repeated laryngoscopies or CT scans revealed no recurrence or residual lesion during the post-surgical course.

[miR-141-3p enhances the proliferation, invasion and migration of CNE-2 human nasopharyngeal carcinoma cells by promoting vimentin expression].

Objective To investigate whether miR-141-3p promote the migration of CNE-2 human nasopharyngeal carcinoma (NPC) cells by regulating vimentin. Methods Real-time quantitative PCR was used to detect the expression of miR-141-3p in NPC tissues and adjacent tissues and the expression level of vimentin was detected by immunohistochemical staining and Western blot analysis. Real-time quantitative PCR and Western blot were used to screen 5-8F, CNE-2, HNE1 human NPC cell lines with the highest relative expression of miR-141-3p. Real-time quantitative PCR and Western blot analysis were used together to verify the relationship between miR-141-3p and vimentin expression. Small interfering RNA (si-miR-141-3p) was used to down-regulate miR-141-3p of CNE-2 cells. MTT assay tested the proliferating inhibition rate of CNE-2 cells. TranswellTM chamber assay was performed to detect cell invasion and migration and Western blot analysis to detect the expression of vimentin. Results Compared with the paracancerous tissues, the expression of miR-141-3p and vimentin in NPC tissues increased significantly. Compared with NP69 cells, the expressions of miR-141-3p and vimentin increased significantly in CNE-2 cells. The down-regulation of miR-141-3p in CNE-2 cells has induced significant decrease of cell invasion and migration capabilities, cell proliferation capabilities, as well as vimentin protein expression. Conclusion miR-141-3p can enhance the proliferation and migration of CNE-2 cells by promoting vimentin expression.

Oxidation and Reduction Dual-Responsive Polymeric Prodrug Micelles Co-delivery Precisely Prescribed Paclitaxel and Honokiol for Laryngeal Carcinoma Combination Therapy.

Laryngeal carcinoma is the most common head and neck malignancy globally, and chemotherapy is still the most common treatment for this type of carcinoma. Monotherapy has become powerless because of the lack of drugs in the anticancer agent library, the difficult process of new drug discovery, and the widespread drug resistance. Combination therapy with two agents, in particular Chinese herbal medicines with chemotherapy drugs, is a potential alternative to chemotherapy alone. However, combination therapy faces difficulties in delivering multiple drugs to tumor tissue in a precise ratio. Here, a cocktail polymeric prodrug micelle (PHPPM) was developed using an oxidation and reduction dual-responsive polymeric paclitaxel (PTX) and polymeric honokiol (HK) prodrugs. Both of them were obtained by covalently conjugating the drug to dextran via diselenium bonds. Following optimization and characterization, the PHPPM with the precise mass ratio of PTX and HK was obtained, enabling ratiometric drug loading, synchronized drug release in response to tumor high-level reactive oxygen species and glutathione environment, long blood circulation, and high tumor accumulation. This co-delivery system can effectively inhibit laryngeal carcinoma growth in vitro and in vivo. Codelivery of chemotherapy agents and Chinese herbal medicine with a precise ratio and controlled release of the two drugs at the tumor site provides an effective approach to clinical therapy for other laryngeal carcinomas.

[Down-regulation of tripartite motif containing 59 (TRIM59) blocks the NF-κB signaling pathway and inhibits the invasion and migration of nasopharyngeal carcinoma cells].

Objective To investigate whether tripartite motif containing 59 (TRIM59) influences the biological behavior of nasopharyngeal carcinoma cells by regulating the nuclear factor κB(NF-κB) signaling pathway. Methods TCGA database was used to predict the expression of TRIM59 in nasopharyngeal carcinoma and adjacent tissues. Reverse transcription PCR and Western blot were used to detect the relative expressions of TRIM59 mRNA and protein in nasopharyngeal carcinoma and paracancerous tissues. With human normal nasal mucosal epithelial cells (HNEpCs) as a control, reverse transcription PCR and Western blot analysis were used to detect the relative expression of TRIM59 mRNA and protein in HNE1 and CNE-2Z nasopharyngeal carcinoma cells. Small interference RNA technology was used to down-regulate the level of TRIM59 in HNE1 cells, while a control group, small interference RNA negative control (si-NC) group and TRIM59 small interference RNA (si-TRIM59) group were set up. MTT assay was used to detect the cell proliferation inhibition rate of each transfection group. TranswellTM chamber was used to detect cell invasion and migration ability of each transfection group. Western blot analysis was employed to detect NF-κB and phosphorylated NF-κB (p-NF-κB), vimentin, survivin protein expression. ELISA was adopted to detect interleukin 6 (IL-6), IL-8, tumor necrosis factor α (TNF-α) in the supernatant of cultured cells. Results The expression of TRIM59 increased abnormally in nasopharyngeal carcinoma tissues. Compared with HNEpC cells, the relative expression of TRIM59 in HNE1 significantly increased. After down-regulating the expression of TRIM59 in HNE1 cells, cell survival and cell invasion and migration were significantly inhibited. Down-regulating the expression of TRIM59 inhibited HNE1 cells p-NF-κB, vimentin, survivin protein expression and significantly reduced the levels of IL-6, IL-8, and TNF-α. Conclusion Down-regulation of TRIM59 blocks the NF-κB signaling pathway and tumor inflammation-related factors in HNE1 cells, thereby inhibiting cell invasion and migration.

[Corrigendum] 3­Bromopyruvate sensitizes human breast cancer cells to TRAIL­induced apoptosis via the phosphorylated AMPK­mediated upregulation of DR5.

Following the publication of this article, an interested reader drew to the authors' attention that the western blotting data shown in Fig. 3 on. p. 2439 contained apparent anomalies; first, the protein bands shown to represent the CHOP and p­AMPK experiments in Fig. 3A were strikingly similar. Secondly, the same data bands were inadvertently included in the figure to represent the GRP78 and Bax experiments for the MCF­7 group. The authors have re­examined their original data and realized that this figure was assembled incorrectly (the CHOP and GRP78 data were inadvertently duplicated in the figure). The corrected version of Fig. 3, showing the correct data for the p­AMPK and Bax experiments for the MCF­7 group in Fig. 3A, is shown on the next page. The authors sincerely apologize for the error that was introduced during the preparation of this figure, thank the Editor of Oncology Reports for granting them the opportunity to publish a Corrigendum, and are grateful to the reader for alerting them to this issue. The authors also regret any inconvenience that this mistake may have caused. [the original article was published in Oncology Reports 40: 2435­2444, 2018; DOI: 10.3892/or.2018.6644].

3­Bromopyruvate sensitizes human breast cancer cells to TRAIL­induced apoptosis via the phosphorylated AMPK­mediated upregulation of DR5.

Previous studies have indicated that the sensitivity of breast cancer cells to tumor necrosis factor­related apoptosis­inducing ligand (TRAIL)­induced apoptosis is associated with the expression of death receptors on the cell membrane. However, drug resistance limits the use of TRAIL in cancer therapy. Numerous studies have indicated that death receptors, which induce apoptosis, are upregulated by the endoplasmic reticulum (ER) stress response. 3­Bromopyruvate (3­BP), an anticancer agent, inhibits cell growth and induces apoptosis through interfering with glycolysis. In the present study, it was demonstrated that 3­BP synergistically sensitized breast cancer cells to TRAIL­induced apoptosis via the upregulation of death receptor 5 (DR5). Furthermore, we found that the protein levels of glucose­related protein 78 (GRP78) and CCAAT­enhancer­binding protein homologous protein (CHOP) increased following treatment with 3­BP. The expression of Bax (in MCF­7 cells) and caspase­3 (in MDA­MB­231 cells) increased following co­treatment with 3­BP and TRAIL, whereas the expression of the anti­apoptotic protein Bcl­2 decreased. In order to investigate the molecular mechanism regulating this effect, the expression of adenosine monophosphate­activated protein kinase (AMPK), activated by 3­BP, was determined. It was demonstrated that phosphorylated­AMPK was upregulated following treatment with 3­BP. Notably, Compound C, an AMPK inhibitor, reversed the effects of 3­BP. Finally, a synergistic antitumor effect of 3­BP and TRAIL was observed in MCF­7 cell xenografts in nude mice. In conclusion, these results indicated that 3­BP sensitized breast cancer cells to TRAIL via the AMPK­mediated upregulation of DR5.

[One-stage repair of pharyngeal defect using tongue flaps after resection of advanced stage hypopharyngeal neoplasm and laryngeal neoplasm].

OBJECTIVE: To study the effectiveness of one-stage repairing pharyngeal defect with the tongue flaps after resection of advanced stage hypopharyngeal neoplasm and laryngeal neoplasm. METHODS: Between June 2006 and March 2011, 20 patients with hypopharyngeal neoplasm (8 cases) and laryngeal neoplasm (12 cases) with advanced stage were treated. There were 19 males and 1 female, aged 47-78 years (mean, 62.8 years). All neoplasms were squamous cell carcinomas. The disease duration was 1-8.5 months (mean, 3.9 months). According to the standards of International Union Against Cancer (UICC, 1987), 12 cases were in stage III and 8 cases were in stage IV. The size of pharyngeal defect was 5 cm x 2 cm to 4 cm x 4 cm after resection of tumor. Defects were repaired by the whole base of the tongue flaps in 16 cases and by the horizontal base of the tongue flaps in 4 cases. The size of the flaps ranged from 5 cm x 2 cm to 4 cm x 4 cm. Postoperative radiotherapy and chemotherapy were regularly performed. RESULTS: The 20 tongue flaps were alive. Healing of incision by first intention was achieved in 18 cases and delayed healing in 2 cases because of subcutaneous fluid. The patients were followed up 12-63 months (mean, 36.7 months). The patients had normal feeding ability and tongue function. Of 20 cases, 12 died and 1 of local recurrence was alive with tumor. The 3-year survival rate was 69.2% (9/13). CONCLUSION: One-stage repair of pharyngeal defect with the tongue flaps after resection of hypopharyngeal neoplasm and laryngeal neoplasm can obtain good effectiveness because the tongue flap is easy-to-obtain and easy-to-survive, and has abundant blood supply.