Pancreatic ductal adenocarcinoma (PDAC) remains one of the most common causes of cancer-related death. Recently, long noncoding RNAs (lncRNAs) have emerged as significant regulators in numerous cancers, including PDAC. LncRNA small nucleolar RNA host gene 1 (SNHG1) has been reported in the development of several tumors, but the biological roles of it in PDAC remain to be illuminated. This study aims to investigate the function of lncRNA SNHG1, revealing its molecular mechanism and clinical significance in PDAC. Herein, we found that SNHG1 was highly expressed in PDAC tissues in comparison with adjacent noncancerous tissues, being closely related to tumor size and TNM stage. Functionally, silencing of SNHG1 could significantly inhibit cell proliferation, promote cell apoptosis, as well as alter cell cycle progression, whereas the contrary results could be presented in the overexpression of SNHG1. In addition, in vivo xenograft experiment also further confirmed the above results. Finally, an activator (740Y-P) and inhibitor (LY294002) of the PI3K/AKT signaling pathway were used in the western blot assays and the following rescue experiments, demonstrating that SNHG1 facilitates cell proliferation and tumorigenicity partly via the PI3K/AKT signaling pathway in PDAC. Hence, SNHG1 may be a prospective therapeutic target.

Background: Pancreatic cancer (PC) is an aggressive malignancy and has a poor prognosis. Although emerging research has revealed that circular RNAs (circRNAs) are crucial modulators that control tumor development and metastasis, their functional involvement in PC has not been well characterized. Here, we examined whether and how circRNA circ_0001666 governs epithelial-mesenchymal transition (EMT) in PC.Methods: We investigated the effects of circ_0001666 on EMT and PC cell invasion by gain- and loss-of-function assays. We also explored the mechanisms underlying the functions of circ_0001666 in PC cells.Results: We found that circ_0001666 is highly expressed in PC tissues and PC cell lines. Patients with high circ_0001666 expression had shorter survival times. In vitro and in vivo experiments have demonstrated that upregulation of circ_0001666 facilitates PC cell proliferation, EMT and invasiveness, whereas knockdown of circ_0001666 exhibits opposite functions. Moreover, circ_0001666 is able to bind to miR-1251, thus increasing the expression of SOX4, which is a direct downstream effector of miR-1251. The oncogenic effects of circ_0001666 on EMT and PC cell invasion were rescued by miR-1251 overexpression.Conclusions: These results suggested that circ_0001666 acts as an oncogenic circRNA to promote EMT and invasion of PC cells through sponging miR-1251, and indicated that circ_0001666 could be explored as a potential therapeutic target for PC.

Mitochondrial ribosomal protein L7/L12 (MRPL12) is a member of the mitochondrial ribosomal proteins (MRPs). However, the biological function of MRPL12 in lung adenocarcinoma (LUAD) remains unclear. The expression and prognostic value of MRPL12 in LUAD were systematically analyzed using UALCAN, TIMER, HPA, Kaplan–Meier plotter, and GEPIA databases. The relationship between MRPL12 and immune infiltrates was investigated using TIMER and TISIDB databases. The clinical significance of MRPL12 in LUAD patients was validated using a tissue microarray (TMA). Cellular functional experiments were carried out to examine the influences of MRPL12 knockdown on cell proliferation, migration, and invasion. MRPL12 was significantly upregulated in LUAD samples, and high MRPL12 expression was correlated with worse prognosis. MRPL12 expression was markedly associated with immunomodulators, chemokines, and infiltration levels of multiple immune cells. Furthermore, TMA results confirm the upregulation of MRPL12 expression in LUAD, and MRPL12 was identified as an independent prognostic factor in LUAD patients. MRPL12 knockdown inhibited proliferation, migration, and invasion of LUAD cells. These data indicate that MRPL12 is a prognostic biomarker and correlated with immune infiltrates in LUAD. Therefore, MRPL12 shows potential as a therapeutic target for LUAD.

Purpose: The NCCN guidelines do not recommend surgery for T3–4N0M0/T1–4N1–2M0 small cell lung cancer (SCLC) due to a lack of evidence. Methods: Data of patients with T3–4N0M0/T1–4N1–2M0 SCLC were extracted from the Surveillance, Epidemiology, and End Results (SEER) database to determine the impact of surgery on this population. The Kaplan–Meier method, univariable and multivariable Cox proportional hazard regression, and propensity score matching (PSM) were used to compare the overall survival (OS) between the surgery and non-surgery groups. In addition, we explored whether sublobectomy, lobectomy, and pneumonectomy could provide survival benefits. Results: In total, 8572 patients with SCLC treated without surgery and 342 patients treated with surgery were included in this study. The PSM-adjusted hazard ratio (HR, 95% CI) for surgery vs. no surgery, sublobectomy vs. no surgery, lobectomy vs. no surgery, pneumonectomy vs. no surgery, and lobectomy plus adjuvant chemoradiotherapy vs. chemoradiotherapy were 0.71 (0.61–0.82) (P < 0.001), 0.91 (0.70–1.19) (P = 0.488), 0.60 (0.50–0.73) (P < 0.001), 0.57 (0.28–1.16) (P = 0.124), and 0.73 (0.56–0.96) (P = 0.023), respectively. The subgroup analysis demonstrated consistent results. Conclusions: Lobectomy improved OS in patients with T3–4N0M0/T1–4N1–2M0 SCLC, while pneumonectomy also demonstrated a tendency to improve OS without statistical significance; however, sublobectomy showed no survival benefit.