[Retracted] lncRNA XIST promotes the progression of laryngeal squamous cell carcinoma by sponging miR­144 to regulate IRS1 expression.

The authors wish to retract their research article entitled 'lncRNA XIST promotes the progression of laryngeal squamous cell carcinoma by sponging miR­144 to regulate IRS1 expression', published in Oncology Reports 43: 525­535, 2020. They have found that, having repeated several of the experiments, XIST expression does not appear to affect LSCC cell apoptosis. In addition, some of their original data had been lost due to computer damage. Therefore, all authors are in agreement that this paper published in Oncology Reports should be retracted to maintain the integrity of the scientific record. All the named authors on the paper agree to this retraction, and they sincerely apologize for any inconvenience that might result from the retraction of this article. [the original article was published in Oncology Reports 43: 525­535, 2020; DOI: 10.3892/or.2019.7438].

Laryngeal myxoma: A case report.

BACKGROUND: Myxomas are benign tumors of mesenchymal origin that rarely occur in the larynx. CASE SUMMARY: We report a case of a laryngeal myxoma that presented as a right vocal cord mass in a 54-year-old man. CONCLUSION: Laryngeal myxoma is a rare benign tumor in the larynx. It is difficult to distinguish glottis myxoma from vocal cord polyps on laryngoscopy. We recommend that otolaryngologists acquire a better understanding of this disease. If a laryngeal myxoma is suspected, dynamic laryngoscopy, acoustic voice analysis, and pathological biopsy should be performed.

lncRNA XIST promotes the progression of laryngeal squamous cell carcinoma by sponging miR­144 to regulate IRS1 expression.

The initiation and development of several types of cancer have been linked to long non­coding RNA (lncRNA) X inactive­specific transcript (XIST). Yet, the pattern of expression, function, as well as the molecular mechanism underlying XIST in laryngeal squamous cell carcinoma (LSCC) lack characterization. Therefore, the present study aimed to determine the function and putative mechanism of XIST in the development of LSCC. It was revealed that the level of XIST was significantly higher in LSCC tissues that were associated with advanced Tumor­Node­Metastasis (TNM) stage and the presence of lymph node metastasis. Furthermore, the ability of human LSCC TU212 cells to proliferate, form colonies, migrate and invade was significantly suppressed, while cell apoptosis was significantly increased following knockdown of XIST. Further investigation revealed that XIST knockdown increased the expression of microRNA­144 (miR­144) by acting as an endogenous sponge of miR­144. Inhibition of miR­144 caused a partial reversal of the inhibitory effects mediated following depletion of XIST in LSCC cells. Moreover, an miR­144 target called insulin receptor substrate 1 (IRS1) was significantly decreased by XIST depletion in LSCC cells. IRS1 expression was positively correlated with XIST expression in LSCC tissues. In addition, knockdown of XIST impaired tumor growth in vivo by regulating the miR­144/IRS1 axis. The present study demonstrated that the progression of LSCC is promoted by XIST sponging miR­144 to regulate IRS1 expression, suggesting that XIST can serve as a putative target in the therapy of LSCC.

miR-144 suppresses the growth and metastasis of laryngeal squamous cell carcinoma by targeting IRS1.

Increasing evidence has been suggested that microRNA-144 (miR-144) involved in tumor initiation, development and metastasis in various cancers. However, the biological roles and potential mechanisms of miR-144 in laryngeal squamous cell carcinoma (LSCC) remain unclear. In the present study, we discovered that miR-144 expression levels in LSCC tissues were significantly lower than those of adjacent normal tissues. Furthermore, overexpression of miR-144 in LSCC cells inhibited cell proliferation, colony formation, migration, and invasion in vitro. Consistently, stable overexpression of miR-144 suppressed the growth of LSCC cell xenografts in vivo. Bioinformatic algorithms and luciferase reporter assays confirmed that insulin receptor substrate 1 (IRS1) is a direct target of miR-144. Overexpreesion of miR-144 obviously decreased IRS1 expression thereby suppressing phosphatidylinositol 3-kinase (PI3K)/AKT pathway activation. Further functional studies suggested that downregulation of IRS1 had similar effects as that of miR-144 overexpression, and upregulation of IRS1 partially reversed the inhibitory effects of miR-144. These findings suggested that miR-144 functioned as a tumor suppressor in LSCC by targeting IRS1, and that miR-144 might serve as a potential target for LSCC treatment.

Papillary thyroid carcinoma and laryngeal squamous cell carcinoma manifesting as a collision tumor of the neck: A case report.

A 55-year-old male presented with a rapidly expanding mass on the right side of the neck and progressive hoarseness. An electronic laryngoscopy and a computed tomography scan were performed, and the patient was subsequently diagnosed with tumors of the larynx and the thyroid gland. An en bloc near-total thyroidectomy combined with a total laryngectomy was performed. The final pathological analysis revealed a collision tumor that was derived from a laryngeal squamous cell carcinoma and a papillary thyroid carcinoma. Collision tumors of the head and neck are rare. The therapy for a collision tumor should consist of a combination of the treatments that are normally used for each focus.