Anlotinib plus oral fluoropyrimidine S-1 in refractory or relapsed small-cell lung cancer (SALTER TRIAL): a multicenter, single-arm, phase II trial.

BACKGROUND: Patients with small-cell lung cancer (SCLC) have few treatment options and dismal overall survival (OS) after failed platinum-based chemotherapy. METHODS: The eligibility criteria of this phase II clinical trial included patients with measurable disease, age of 18 to 75 years, a confirmed diagnosis of disease progression or recurrence after prior platinum-based chemotherapy with a pathologically proven diagnosis of SCLC. Patients were treated with anlotinib at a dosage of 12 mg once daily (QD) and S-1 at 60 mg twice daily (BID) for 2 weeks, followed by a 1-week treatment-free interval. After six cycles of the above treatment, patients continued the maintenance therapy using S-1 monotherapy at 60 mg/ BID for 2 weeks, followed by a 1-week treatment-free interval until disease progression. RESULTS: From March 2019 to June 2020, a total of 71 patients were initially assessed for eligibility in this study. Out of these, 52 patients who met the inclusion criteria were enrolled, and 48 patients received at least two doses of the study drug. The median follow-up time was 25.1 months. The ORR was seen in 21 patients (43.8%). The median PFS was 4.5 months (95% CI, 3.5-5.5 months), and the median OS was 5.9 months (95% CI, 4.6-7.3 months). The most common grade 3-4 treatment-related adverse events were thrombocytopenia (16.7%), anemia (14.6%), neutropenia (14.6%), and hypertension (10.4%). No treatment-related death occurred. CONCLUSIONS: The combination of anlotinib with oral fluoropyrimidine S-1 demonstrated notable activity in relapsed or refractory SCLC, showing a favorable ORR and an acceptable, manageable safety profile. TRIAL REGISTRATION: This trial was registered with ClinicalTrial.gov (NCT03823118) on 3 January 2019.

[Retracted] MicroRNA­671­5p inhibits cell proliferation, migration and invasion in non­small cell lung cancer by targeting MFAP3L.

Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that the western blotting data shown in Fig. 4B and the Transwell cell invasion data shown in Figs. 2D and 4E were strikingly similar to data appearing in different form in other articles written by different authors at different research institutes that had already been published elsewhere prior to the submission of this paper to Molecular Medicine Reports (one of which has been retracted). Moreover, there appeared to be inappropriately edited western blot bands featured in Figs. 4 and 5. In view of the fact that certain of the abovementioned data had already apparently been published previously, the Editor of Molecular Medicine Reports has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they agreed with the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 25: 30, 2022; DOI: 10.3892/mmr.2021.12546].

MicroRNA­671­5p inhibits cell proliferation, migration and invasion in non­small cell lung cancer by targeting MFAP3L.

MicroRNA (miR)­671­5p serves as a tumor suppressor in several types of cancer, including gastric and breast cancer. However, the function of miR­671­5p in non­small cell lung cancer (NSCLC) has not been described in detail. The present study aimed to investigate the role of miR­671­5p in NSCLC. The expression levels of miR­671­5p were determined in NSCLC tissue samples and cell lines using reverse transcription­quantitative PCR. Prediction of miR­671­5p targets was performed using the TargetScan database and verified by luciferase reporter assay and western blot analysis. Functional experiments, including Cell Counting Kit­8, wound healing and Transwell assays, were performed in NSCLC cells. The results of the present study demonstrated that lower expression levels of miR­671­5p were observed in NSCLC tissues and cell lines compared with those in the corresponding controls. Low miR­671­5p levels were significantly associated with an advanced Tumor­Node­Metastasis stage and lymph node metastasis in patients with NSCLC. Microfibril­associated protein 3­like (MFAP3L) was confirmed to be a direct target of miR­671­5p. The proliferative, migratory and invasive abilities of NSCLC cells were suppressed following transfection with miR­671­5p mimics and promoted by the miR­671­5p inhibitor compared with those in the respective control groups. In addition, the effects of miR­671­5p on cell proliferation, migration and invasion, as well as the expression levels of proliferating cell nuclear antigen, E­cadherin, N­cadherin and vimentin were reversed by MFAP3L overexpression. In conclusion, targeting the miR­671­5p/MFAP3L signaling pathway may be a promising therapeutic strategy for NSCLC treatment.