scholarly journals Mechanosensitive Channel Piezo1 Induces Cell Apoptosis in Pancreatic Cancer by Ultrasound with Microbubbles

iScience ◽  
2022 ◽  
pp. 103733
Author(s):  
Yue Song ◽  
Jifan Chen ◽  
Cong Zhang ◽  
Lei Xin ◽  
Qunying Li ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Apoptosis ◽  
Mechanosensitive Channel

scholarly journals Paeoniflorin inhibits human pancreatic cancer cell apoptosis via suppression of MMP-9 and ERK signaling

2016 ◽  
Vol 12 (2) ◽  
pp. 1471-1476 ◽  
Author(s):  
Nanmu Yang ◽  
Hong Cui ◽  
Feng Han ◽  
Ling Zhang ◽  
Tao Huang ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cell ◽  
Cell Apoptosis ◽  
Pancreatic Cancer Cell ◽  
Erk Signaling ◽  
Human Pancreatic Cancer ◽  
Human Pancreatic Cancer Cell ◽  
Cancer Cell Apoptosis

scholarly journals LINC01121 Inhibits Cell Apoptosis While Facilitating Proliferation, Migration, and Invasion Though Negative Regulation of the Camp/PKA Signaling Pathway via GLP1R

2018 ◽  
Vol 47 (3) ◽  
pp. 1007-1024 ◽  
Author(s):  
Yi-Gang Qian ◽  
Zhou Ye ◽  
Hai-Yong Chen ◽  
Zhen Lv ◽  
Ai-Bin Zhang ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Microarray Data ◽  
Cell Apoptosis ◽  
Migration And Invasion ◽  
Protein Levels ◽  
Pancreatic Cancer Cells ◽  
Significant Difference

Background/Aims: Pancreatic cancer is an aggressive malignancy as a result of highly metastatic potential. The current study was carried out to alter the expression of LINC01121 in pancreatic cancer, with the aim of elucidating its effects on the biological processes of cell proliferation, migration, invasion, and apoptosis. We hypothesized that both the GLP1R gene and cAMP/PKA signaling pathway participate in the aforementioned process. Methods: Microarray data (GSE14245, GSE27890 and GSE16515) and annotating probe files linked to pancreatic cancer were downloaded through the GEO database. The Multi Experiment Matrix (MEM) site was used to predict the target gene of lncRNA. Both pancreatic cancer tissues (n = 56) and paracancerous tissues (n = 45) were collected from patients diagnosed with pancreatic cancer. Immunohistochemistry was applied to identify the positive expression rate of GLP1R protein. Isolated pancreatic cancer cells and PANC-1 cells were independently classified into the blank, negative control (NC), LINC01121 vector, siRNA-LINC01121, siRNA-GLP1R and siRNA-LINC01121 + siRNA-GLP1R groups. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blot analysis were applied to detect the expressions of LINC01121, GLP1R, cAMP, PKA, CREB, Bcl-2, Bad and PCNA. Cell proliferation, migration, invasion, cycle progression, and apoptosis were examined by MTT assay, scratch test, Transwell assay and flow cytometry analyses of Annexin V-FITC/PI staining. Results: Observations were made indicating that LINC01121 was highly expressed, while low expressions of GLP1R in pancreatic cancer were detected based on microarray data, which was largely in consistent with the data collected of LINC01121 and GLP1R within the tissues. The target prediction program and luciferase activity analysis was testament to the notion suggesting that GLP1R was indeed a target of LINC01121. In contrast to the blank and NC groups, the LINC01121 vector group exhibited increased expressions of LINC01121; decreased mRNA and protein levels of GLP1R, Bad, cAMP, and PKA; increased protein levels of CREB, Bcl-2, PCNA, p-PKA and p-CREB; increased cell proliferation, migration and invasion; and decreased cell apoptosis. There was no significant difference detected among the blank, NC, and siRNA-LINC01121 + siRNA-GLP1R groups, except that decreased LINC01121 expression was determined in the siRNA-LINC01121 + siRNA-GLP1R group. Parallel data were observed in the pancreatic cancer cells and PANC-1 cells. Conclusion: The current study presents evidence indicating that LINC01121 might inhibit apoptosis while acting to promote proliferation, migration, and invasion of pancreatic cancer cells, supplementing the stance held that LINC01121 functions as a tumor promoter by means of its involvement in the process of translational repression of the GLP1R and inhibition of the cAMP/PKA signaling pathway.

scholarly journals GINS2 affects cell viability, cell apoptosis, and cell cycle progression of pancreatic cancer cells via MAPK/ERK pathway

2020 ◽  
Vol 11 (16) ◽  
pp. 4662-4670
Author(s):  
Miao Zhang ◽  
Saifei He ◽  
Xing Ma ◽  
Ying Ye ◽  
Guoyu Wang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Pancreatic Cancer ◽  
Cell Viability ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Cell Cycle Progression ◽  
Erk Pathway ◽  
Cycle Progression ◽  
Pancreatic Cancer Cells

scholarly journals The Ibr-7 Derivative of Ibrutinib Exhibits Radiosensitivity in Pancreatic Cancer Cells via Targeting EGFR

2020 ◽  
Author(s):  
Biqin Tan ◽  
Bo Zhang ◽  
Youyou Yan ◽  
Qingyu Li ◽  
Fei Wang ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Human Pancreatic Cancer ◽  
Dependent Manner ◽  
Immunofluorescence Analysis ◽  
Proliferative Effect ◽  
Pancreatic Cancer Cells ◽  
Radiation Group ◽  
M Phase

Abstract Background: Radiotherapy is one of the main therapeutic methods for pancreatic cancer, but radiation resistance limits the clinical application. As a result, novel therapeutic agents to improve the radiosensitivity is urgent. This study aimed to investigate the effect of Ibr-7 (the derivative of ibrutinib) on radiosensitivity of human pancreatic cancer cells.Methods: The effect of Ibr-7 on pancreatic cancer cell’s proliferation were detected by CCK-8 assay. Radiosensitivity was assessed by clonogenic formation assay. Cell cycle, cell apoptosis were analyzed by flow cytometry. DNA damage was detected by immunofluorescence analysis. The expression of p-EGFR, EGFR were determined by western blot.Results: Ibr-7 showed anti-proliferative effect in PANC-1 and Capan2 cells in a dose- and time-dependent manner. Ibr-7 (2 µmol/L) enhanced the effect of radiation in PANC-1 and Capan2 cells. Further findings showed that this combination enhanced G2/M phase arrest and increased cell apoptosis. Additional molecular mechanism studies revealed that the expression of p-EGFR was decreased by Ibr-7 alone or combined with radiation. Overexpression of EGFR reversed the cell apoptosis induced by Ibr-7 combined with radiation. Moreover, the expression of γ-H2AX was significantly decreased in Ibr-7 combined with radiation group.Conclusions: Our study indicated that the potential application of Ibr-7 as a highly effective radiosensitizer for the treatment of pancreatic cancer cells.

scholarly journals Retraction Note to: Excessive mitochondrial fragmentation triggered by erlotinib promotes pancreatic cancer PANC‑1 cell apoptosis via activating the mROS‑HtrA2/Omi pathways

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Jun Wan ◽  
Jie Cui ◽  
Lei Wang ◽  
Kunpeng Wu ◽  
Xiaoping Hong ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Apoptosis ◽  
Mitochondrial Fragmentation

The authors have retracted this article [1] because Figure 4a has been duplicated from Figure 5d in a previously published article [2]. In addition, the article contains sections that substantially overlap with the following articles (amongst others) [3–5]. The data reported in this article are therefore unreliable. Author Hong Ke stated on behalf of all co-authors that they agree to this retraction.

scholarly journals Regulation of cell apoptosis and proliferation in pancreatic cancer through PI3K/Akt pathway via Polo-like kinase 1

2016 ◽  
Vol 36 (1) ◽  
pp. 49-56 ◽  
Author(s):  
YONGHUAN MAO ◽  
LING XI ◽  
QUAN LI ◽  
ZELING CAI ◽  
YIMEI LAI ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Apoptosis ◽  
Akt Pathway
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