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Additional file 15: Table S4. The possible TFO and TTS predicted for PLACT1 and IκBα promoter.

Additional file 7: Figure S5. hnRNPA1 is required for PLACT1-induced PDAC progression.

Additional file 2.

Additional file 10: Figure S8. PLACT1 forms a positive feedback loop with E2F1.

Additional file 9: Figure S7. PLACT1 forms triplexes with promoter sequences of IκBα and regulates its expression.

Additional file 9: Table S2. Oligonucleotide sequences for this study.

Additional file 1: Supplementary material and methods.

Additional file 1.

Additional file 2: Figure S1. The identification of PLACT1 in PDAC.

Additional file 4.

Additional file 3: Table S1. Univariate and multivariate analysis of disease-free survival in PDAC patients.

Additional file 13: Table S3. Antibodies of experiments.

Additional file 5: Figure S3. PLACT1 enhances proliferation, migration, and invasion of PDAC cells.

Additional file 10: Table S1. Primers used in PCR.

Pancreaticoduodenectomy is the only possible surgical procedure for the cure of pancreatic head carcinoma. With the development of minimally invasive surgery, the minimally invasive surgical treatment of pancreatic head carcinoma has become more mature, and an increasing number of grade A tertiary hospitals have reported the minimally invasive surgery for pancreatic head carcinoma. With reference to related articles and experience of our center for pancreatic surgery, this article elaborates on the current status of minimally invasive surgical treatment of pancreatic head carcinoma and points out the perspectives and development directions of minimally invasive treatment of pancreatic head carcinoma

Additional file 4. uncropped blot for Fig. S3A and Fig. 3B.

Additional file 1: Fig. S1 to Fig. S6 and Table S1 to Table S5. Supplementary figures and Tables.

Additional file 12: Table S2. Primer and probes of experiments.

Additional file 4 Figure S1. The identification of the downstream targets of miR-486-5p.

Additional file 8 Figure S2. Full uncut original pictures.

Additional file 6 Table S4. Univariate and multivariate analyses of DFS for circNFIB1 expression in PDAC patients.

Additional file 6: Figure S4. PLACT1 promotes proliferation, migration, and invasion of PDAC cells independent of KRAS/p53.

Additional file 3. Supplementary methods.

Additional file 9 Figure S3. Full uncut original gels.

Additional file 14: Figure S9. Full uncut original pictures.

Additional file 2 Table S2. Primers and probes used in the experiments.

Additional file 7 Table S5. Antibodies used in the experiments.

Additional file 1 Table S1. Correlation between circNFIB1 expression and clinicopathologic characteristics of PDAC patients

Additional file 5 Table S3. Univariate and multivariate analyses of OS for circNFIB1 expression in PDAC patients.

Additional file 8: Figure S6. PLACT1 induces activation of the NF-κB signaling pathway in an IκBα-dependent manner.

Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy. Long non‐coding RNAs (lncRNAs) are important regulators in pathological processes, yet their potential roles in PDAC are poorly understood. Here, we identify a fundamental role for a novel lincRNA, linc00511, in the progression of PDAC. Linc00511 levels in PDAC tissue specimens and cell lines were examined by quantitative real‐time PCR. Corresponding adjacent non‐neoplastic tissues were used as controls. The function of linc00511 in PDAC cell lines was determined by RNA interference approach in vitro and in vivo. Fluorescence in situ hybridization (FISH) was used to characterize linc00511 expression in PDAC cells. Insights of the mechanism of competitive endogenous RNAs (ceRNAs) were obtained from bioinformatic analysis, luciferase assays and RIP assays. The association between the linc00511/hsa‐miR29b‐3p axis and VEGFA was verified by Western blotting assay. Immunohistochemistry was performed to evaluate the expression of VEGFA in PDAC samples. The aberrant up‐regulation of linc00511 was detected in PDAC cell lines and patient specimens compared with controls. An increase in linc00511 expression indicates the adverse clinical pathological characteristics and poor prognosis. Functionally, linc00511 depletion in PDAC cells decreased proliferation, migration, invasion and endothelial tube formation. Mechanistically, linc00511 could up‐regulate VEGFA via its competing endogenous RNA (ceRNA) activity on hsa‐miR‐29b‐3p. In summary, our results define an important axis controlling proliferation, invasion and tumour angiogenesis in PDAC. Linc00511 is a novel lncRNA that plays a significant regulatory role in the pathogenesis and progression of PDAC. Thus, Linc00511 represents a new prognostic biomarker to predict clinical outcome of PDAC patients after surgery and may serve as a potential therapeutic target for PDAC treatment.

Supplemental Digital Content is available in the text, Several reports suggest that gemcitabine (GEM) plus S-1 combination (GS) is associated to prolong the survival in patients with unresectable pancreatic cancer (PC). We conducted a systemic review and meta-analysis of studies comparing the safety and efficacy of GS versus GEM. Summary data from randomized trials and retrospective studies were searched in PubMed, EMBASE, Web of Science, and the Cochrane Library. Statistical analyses were conducted to calculate the hazard ratios (HRs) and relative risk (RR) with 95% confidence intervals (CIs) using random-effects models. Subgroup analyses based on the chemotherapy cycles were performed to explore the efficacy and toxicity for therapy. Sensitivity analyses were conducted by removing specific studies to assess the effects of study quality. Between January 2004 and August 2012, 4 RCTs and 2 retrospective studies including a total of 1025 cases were identified. The overall survival (OS) (HR: 0.82; 95% CI, 0.70–0.96; P = 0.01) and progression-free survival (PFS) (HR: 0.65; 95% CI, 0.55–0.77; P