Noteworthy prognostic value of phospholipase C delta genes in early stage pancreatic ductal adenocarcinoma patients after pancreaticoduodenectomy and potential molecular mechanisms

Zhou, Xin; Liao, Xiwen; Wang, Xiangkun; Huang, Ketuan; Yang, Chengkun; Yu, Tingdong; Han, Chuangye; Zhu, Guangzhi; Su, Hao; Han, Quanfa; Chen, Zijun; Huang, Jianlv; Gong, Yizhen; Ruan, Guo‐Tian; Ye, Xinping; Peng, Tao

doi:10.1002/cam4.2699

Cited by 11 publications

(7 citation statements)

References 59 publications

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“…In esophageal squamous carcinoma cells, PLCD1 was indicated to inhibit cell proliferation, invasion and migration by suppressing the Wnt/β-catenin signaling pathway ( 22 ). In pancreatic and breast cancer tumors, PLCD1 expression also exerted similar regulatory effects ( 23 – 25 ). Thus, it was hypothesized that the activation of PLCD1 contributed to tumor suppression.…”

Section: Discussionmentioning

confidence: 94%

Origin recognition complex 1 regulates phospholipase Cδ1 to inhibit cell proliferation, migration and epithelial‑mesenchymal transition in lung adenocarcinoma

et al. 2022

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As a common pulmonary malignant disease, lung adenocarcinoma exhibits high mortality and morbidity rate. Phospholipase Cδ1 (PLCD1), an enzyme involved in the homeostasis of energy metabolism, is downregulated in lung adenocarcinoma. According to GEPIA, origin recognition complex 1 (ORC1) is a highly expressed gene in lung adenocarcinoma and is negatively associated with PLCD1. To the best of our knowledge, the present study was the first to investigate the role of ORC1 in regulating PLCD1 in lung adenocarcinoma. According to TCGA database, low expression of PLCD1 was correlated with the low overall survival rate of patients suffering from lung adenocarcinoma. The protein and mRNA expression levels of PLCD1 and ORC1 were detected in A549 cells by western blot analysis and reverse transcription-quantitative PCR, respectively. Cell proliferation, invasion and migration were analyzed by MTT, colony formation, Transwell and wound healing assay. Immunofluorescence staining was adopted to estimate the content of Ki67 and western blot was applied for the evaluation of PLCD1, MMP2, MMP9, E-cadherin, N-cadherin, vimentin, Snail and ORC. The binding interaction between ORC1 and PLCD1 was analyzed using chromatin immunoprecipitation and luciferase reporter enzyme gene assays. The results indicated that PLCD1 was lowly expressed in lung adenocarcinoma cells in comparison with that in 16HBE. When PLCD1 was overexpressed in cancer cells, cell proliferation, invasion and migration were significantly inhibited. However, in the presence of both ORC1 and PLCD1 overexpression, the suppressive effects of PLCD1 overexpression alone on cell proliferation, invasion, migration and EMT were attenuated. In conclusion, ORC1 was indicated to inhibit PLCD1, thus regulating the proliferation, migration and EMT processes of lung adenocarcinoma cells, which suggested that ORC1 might be a target for the treatment of lung adenocarcinoma.

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Section: Discussionmentioning

confidence: 94%

Origin recognition complex 1 regulates phospholipase Cδ1 to inhibit cell proliferation, migration and epithelial‑mesenchymal transition in lung adenocarcinoma

et al. 2022

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“…As was previously described, PLCD3 plays an oncogenic role in a variety of cancers, such as nasopharyngeal, thyroid, and early pancreatic ductal carcinoma [ 8 – 10 ]. However, whether PLCD3 has the same effect on ESCC progression and how it works is unclear.…”

Section: Discussionmentioning

confidence: 95%

“…PLCD3 is a critical metabolic enzyme in the 13 mammalian PLC subtypes, whose function in tumors is not frequently mentioned. It has been reported to be an oncogene in nasopharyngeal and thyroid cancer [ 8 , 9 ] and a prognostic marker for early-stage pancreatic ductal carcinoma [ 10 ]. However, its role in ESCC has not yet been found.…”

Section: Introductionmentioning

confidence: 99%

PLCD3 promotes malignant cell behaviors in esophageal squamous cell carcinoma via the PI3K/AKT/P21 signaling

Wang,

Gao,

Chen

et al. 2023

BMC Cancer

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Background Phospholipase C Delta 3 (PLCD3) is a member of phospholipase C(PLC) Protein and PLCD3 protein plays a prominent role in many cancers. However, little is known about the role of PLCD3 in esophageal squamous cell carcinoma (ESCC). Material and Methods We analyzed PLCD3 mRNA and protein expression in ESCC tissues and cell lines by immunohistochemistry, quantitative real-time PCR, and western blot. The correlation between PLCD3 expression and clinicopathological characteristics was also analyzed. CCK8, colony formation, wound-healing, and transwell assays were conducted to measure cell functional alternations. Flow cytometry was performed to assess the apoptosis rate and cell cycle caused by PLCD3 knockdown. Xenograft models in nude mice to clarify the role of PLCD3 in ESCC. Key proteins in the PI3K / AKT signaling pathway after treatment of ECA109 and KYSE150 cells with the AKT inhibitor MK2206 were analyzed by western blot. Results PLCD3 was highly expressed in ESCC tissues and cell lines. PLCD3 expression levels correlated with pathologic stage and lymphatic metastasis. PLCD3 knockdown inhibited cell proliferation, migration, invasion, promoted apoptosis, and caused the cell cycle arrest in the G1 phase. PLCD3 overexpression promoted cell proliferation, migration, and invasion. In vivo experiments with xenografts demonstrated that PLCD3 promoted ESCC tumorigenesis. Finally, Overexpression of PLCD3 activated the PI3K / AKT / P21 signaling. Conclusion PLCD3 promotes malignant cell behaviors in esophageal squamous cell carcinoma via the PI3K/AKT/P21 signaling and could serve as a potential target for ESCC treatment.

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“…23 The phospholipase PLCD1 (+124-fold change) has previously been found to be significantly overexpressed in PDAC tissues, leading to questions about its possible use as a prognostic marker. 24 The PRUNE gene (+70-fold change) has been described as a promoter of invasion in many cancer types, including PDAC, colorectal, breast, and anaplastic thyroid. 25 Among genes downregulated in PANC-1, Birc-2 (CAP1, −134-fold change) has been identified as a possible antiapoptotic oncogene in PDAC.…”

Section: Discussionmentioning

confidence: 99%

Direct Effects of Lipopolysaccharide on Human Pancreatic Cancer Cells

Massoumi¹,

Teper²,

Ako³

et al. 2021

Pancreas

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Objectives: Obesity, a risk factor for pancreatic adenocarcinoma (PDAC), is often accompanied by a systemic increase in lipopolysaccharide (LPS; metabolic endotoxemia), which is thought to mediate obesity-associated inflammation. However, the direct effects of LPS on PDAC cells are poorly understood. Methods:The expression of toll-like receptor 4, the receptor for LPS, was confirmed in PDAC cell lines. AsPC-1 and PANC-1 cells were exposed to LPS, and differential gene expression was determined by RNA sequencing. The activation of the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway by LPS in PDAC cells was assessed by Western blotting. Results:The expression of toll-like receptor 4 was confirmed in all PDAC cell lines. The exposure to LPS led to differential expression of 3083 genes (426 ≥5-fold) in AsPC-1 and 2584 genes (339 ≥5-fold) in PANC-1. A top canonical pathway affected by LPS in both cell lines was PI3K/Akt/mTOR. Western blotting confirmed activation of this pathway as measured by phosphorylation of the ribosomal protein S6 and Akt. Conclusions:The exposure of PDAC cells to LPS led to differential gene expression. A top canonical pathway was PI3K/Akt/mTOR, a known oncogenic driver. Our findings provided evidence that LPS can directly induce differential gene expression in PDAC cells.

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Noteworthy prognostic value of phospholipase C delta genes in early stage pancreatic ductal adenocarcinoma patients after pancreaticoduodenectomy and potential molecular mechanisms

Cited by 11 publications

References 59 publications

Origin recognition complex 1 regulates phospholipase Cδ1 to inhibit cell proliferation, migration and epithelial‑mesenchymal transition in lung adenocarcinoma

Origin recognition complex 1 regulates phospholipase Cδ1 to inhibit cell proliferation, migration and epithelial‑mesenchymal transition in lung adenocarcinoma

PLCD3 promotes malignant cell behaviors in esophageal squamous cell carcinoma via the PI3K/AKT/P21 signaling

Direct Effects of Lipopolysaccharide on Human Pancreatic Cancer Cells

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