Circular RNA (circRNA) is a new class of non-coding RNA that plays a pivotal role in carcinogenesis. Recently, circ-MTO1 (hsa_circ_0007874) was shown to be a cancer-related circRNA. However, its role in lung adenocarcinoma (LUAD) has not been reported. Here, we found that circ-MTO1 was significantly down-regulated in LUAD, which was closely associated with malignant features and dismal prognosis. Enforced expression of circ-MTO1 suppressed the growth of LUAD cells both in vitro and in vivo. Subsequent mechanism experiments showed that circ-MTO1 served as a sponge of oncogenic miR-17 to increase the expression of RNA-binding protein QKI-5, leading to the inactivation of Notch signaling pathway, thereby restraining the growth of LUAD. Importantly, increased QKI-5 expression caused by circ-MTO1 overexpression in turn promoted circ-MTO1 expression. Clinically, circ-MTO1 expression was strongly positively correlated with QKI-5 expression, but negatively correlated with miR-17 expression. Taken together, our data suggest that circ-MTO1 is a critical negative regulator of LUAD and elucidate the potential molecular mechanism of a novel circ-MTO1/miR-17/QKI-5 feedback loop in inhibiting LUAD progression.

Background: Long non-coding RNAs (lncRNAs) can play pivotal roles in tumor progression by acting as microRNA (miRNA) sponges. This study aimed to investigate the association of a novel lncRNA, TRPM2-AS, with the miR-138-5p/EGFR axis in the development of non-small cell lung cancer (NSCLC).Methods: Sixty NSCLC tissues and paired adjacent non-tumor tissues were analyzed. The relative expression levels of TRPM2-AS, miR138-5p, and epidermal growth factor receptor (EGFR) and the interactions between them were analyzed. The NSCLC cell lines NCI-H1299 and A549 were transfected with TRPM2-AS shRNA/pcDNA, and miR-138-5p mimics. Cell proliferation, migration, invasion, and apoptosis were examined in response to different transfection conditions. Dual-luciferase reporter assay was performed to identify the target interactions between TRPM2-AS, miR-138-5p, and EGFR. A549 cells stably transfected with shRNA were injected into BALB/c null nude mice to establish a tumor xenograft model.Results: TRPM2-AS was up-regulated in NSCLC tumors and cell lines. Cell proliferation, migration, and invasion were inhibited in NSCLC cells treated with sh-TRPM2-AS, while apoptosis was induced.The targeting of TRPM2-AS by miR138-5p and miR138-5p by EGFR were validated with dual-luciferase reporter assay. TRPM2-AS was found to be negatively correlated with miR138-5p but positively correlated with EGFR. PI3K/AKT/mTOR was activated by pcDNA-EGFR but inactivated by miR-138-5p mimics. In the tumor xenograft mouse model, sh-TRPM2-AS suppressed tumor formation, reduced the expression of EGFR and Ki67, and promoted tumor cell apoptosis. Conclusions:Our results suggested that TRPM2-AS can increase the levels of EGFR via sponging miR-138-3p; this promoted NSCLC cell proliferation, migration, and invasion in vitro, and exacerbated tumors in vivo. These findings highlight TRPM2-AS/miR-138-5p as a potential target for reducing drug resistance in patients with NSCLC.

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Pulmonary sclerosing pneumocytoma (PSP) is a rare benign or low-grade malignant tumor, but it has the potential to present with multiple lesions, lymph node metastasis, extra-pulmonary metastasis, recurrence and even cause death. Herein, a case of PSP that was huge, presented with multiple lesions and had lymph node as well as extrapulmonary metastases (liver, abdominal cavity, bones) is reported for the first time. This patient was also the first one to die of respiratory and circulatory failure caused by the PSP tumor and its metastases which compressed the mediastinal tissue.

Objective To analyze the clinical characteristics of patients with malignant pulmonary sclerosing pneumocytoma (PSP) with metastasis, recurrence, and growth and to improve clinicians’ understanding of PSP in patients with malignant tumor characteristics. Methods A total of 46 PSP patients with malignant tumor characteristics were identified in the literature search and compared with 38 patients with benign PSP diagnosed and treated in our hospital in the past 5 years. We explored the pathogenesis, clinical symptoms, diagnostic methods, treatment strategies and prognosis of PSP patients with malignant tumor. Results The characteristics of young age (≤41 years old), larger tumor (≥36mm), lymph node metastasis and distribution in East Asians are indicative of PSP with malignant potential. Such patients should undergo segmental resection or lobectomy, combined with necessary lymph node dissection or biopsy. All patients with PSP should have an entire course of follow-up management, because they may have an adverse prognosis such as recurrence, growth, metastasis, and even death. Conclusion PSP has the potential for malignancy. Anatomical lobectomy or segmental resection combined with lymph node dissection should be performed in PSP with some specific characteristics. Inappropriate diagnosis and treatment may lead to poor prognosis in PSP patients.