RUNX2 and LAMC2: promising pancreatic cancer biomarkers identified by an integrative data mining of pancreatic adenocarcinoma tissues

Jin, Guihua; Ruan, Qingqing; Shangguan, Fugen; Lan, Linhua

doi:10.18632/aging.203589

Cited by 10 publications

(7 citation statements)

References 55 publications

(43 reference statements)

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“…As a unique subunit of LM-332, LAMC2 has been reported to be up-regulated in esophageal squamous cell carcinoma [45] and ovarian carcinoma [46]. In PDAC, the elevated expression of LAMC2 has been detected not only in tumor tissues [47] but also in serum [48]. In addition, LAMC2 has also been identified as an oncogene to promote PDAC progression by modulating EMT-and ATP-binding assiette transporters [49] or EGFR/ERK 1/2 /AKT/mTOR axis [50].…”

Section: Discussionmentioning

confidence: 99%

S100A10 Promotes Pancreatic Ductal Adenocarcinoma Cells Proliferation, Migration and Adhesion through JNK/LAMB3-LAMC2 Axis

Lin

Yang

et al. 2022

Cancers

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Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive tumors, characterized by diagnosis at an advanced stage and a poor prognosis. As a member of the S100 protein family, S100A10 regulates multiple biological functions related to cancer progression and metastasis. However, the role of S100A10 in PDAC is still not completely elucidated. In this study, we reported that S100A10 was significantly up-regulated in PDAC tissue and associated with a poor prognosis by integrated bioinformatic analysis and human PDAC tissue samples. In vitro, down-regulation of S100A10 reduced the proliferation, migration, and adhesion of PDAC cell lines, whereas up-regulation of S100A10 showed the opposite effect. Furthermore, LAMB3 was proved to be activated by S100A10 using RNA-sequencing and western blotting. The effect of LAMB3 on the proliferation, migration, and adhesion of PDAC cells was similar to that of S100A10. Up-regulation or down-regulation of LAMB3 could reverse the corresponding effect of S100A10. Moreover, we validated S100A10 activates LAMB3 through the JNK pathway, and LAMB3 was further proved to interact with LAMC2. Mice-bearing orthotopic pancreatic tumors showed that S100A10 knocked-down PANC-1 cells had a smaller tumor size than the control group. In conclusion, S100A10 promotes PDAC cells proliferation, migration, and adhesion through JNK/LAMB3-LAMC2 axis.

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Section: Discussionmentioning

confidence: 99%

S100A10 Promotes Pancreatic Ductal Adenocarcinoma Cells Proliferation, Migration and Adhesion through JNK/LAMB3-LAMC2 Axis

Lin

Yang

et al. 2022

Cancers

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“…However, most patients with PPAD are already in advanced stages, and they have missed the opportunity for surgical treatment after being diagnosed. The curative impact of radiation and chemotherapy for PAAD is not precise [3]. Considering that molecularly targeted therapy has become an indispensable method of treating malignant tumors, identifying novel therapeutic targets is critical.…”

Section: Introductionmentioning

confidence: 99%

Novel necroptosis-related gene signature for predicting the prognosis of pancreatic adenocarcinoma

Huang

Cai

et al. 2022

Aging

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Pancreatic adenocarcinoma (PAAD) is a deadly digestive system tumor with a poor prognosis. Recently, necroptosis has been considered as a type of inflammatory programmed cell death. However, the expression of necroptosis-related genes (NRGs) in PAAD and their associations with prognosis remain unclear. NRGs' prediction potential in PAAD samples from The TCGA and GEO datasets was investigated. The prediction model was constructed using Lasso regression. Co-expression analysis showed that gene expression was closely related to necroptosis. NRGs were shown to be somewhat overexpressed in high-risk people even when no other clinical symptoms were present, indicating that they may be utilized in a model to predict PAAD prognosis. GSEA showed immunological and tumor-related pathways in the high-risk group. Based on the findings, immune function and m6A genes differ significantly between the low-risk and high-risk groups. MET, AM25C, MROH9, MYEOV, FAM111B, Y6D, and PPP2R3A might be related to the oncology process for PAAD patients. Moreover, CASKIN2, TLE2, USP20, SPRN, ARSG, MIR106B, and MIR98 might be associated with low-risk patients with PAAD. NRGs and the relationship of the immune function, immune checkpoints, and m6A gene expression with NRGs in PAAD may be considered as potential therapeutic targets that should be further studied.

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“…In OSCC, RUNX2 gene silencing abolished the malignant progression, and a reduction in EdU positivity in both CAL-27 and TSCCA cells was observed [ 15 ]. In pancreatic adenocarcinoma, PI3K/AKT and MAPK signaling might be modulated by RUNX2 to augment cell growth [ 16 ]. In colorectal cancer, the cell proliferation markers Ki-67 and PCNA were downregulated upon RUNX2 silencing, and RUNX2 was required for CBFβ-elicited cell proliferation.…”

Section: Runx2 and Cancer Proliferationmentioning

confidence: 99%

RUNX2 and Cancer

Lin

2023

IJMS

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Runt-related transcription factor 2 (RUNX2) is critical for the modulation of chondrocyte osteoblast differentiation and hypertrophy. Recently discovered RUNX2 somatic mutations, expressional signatures of RUNX2 in normal tissues and tumors, and the prognostic and clinical significance of RUNX2 in many types of cancer have attracted attention and led RUNX2 to be considered a biomarker for cancer. Many discoveries have illustrated the indirect and direct biological functions of RUNX2 in orchestrating cancer stemness, cancer metastasis, angiogenesis, proliferation, and chemoresistance to anticancer compounds, warranting further exploration of the associated mechanisms to support the development of a novel therapeutic strategy. In this review, we focus mainly on critical and recent research developments, including RUNX2’s oncogenic activities, by summarizing and integrating the findings on somatic mutations of RUNX2, transcriptomic studies, clinical information, and discoveries about how the RUNX2-induced signaling pathway modulates malignant progression in cancer. We also comprehensively discuss RUNX2 RNA expression in a pancancer panel and in specific normal cell types at the single-cell level to indicate the potential cell types and sites for tumorigenesis. We expect this review to shed light on the recent mechanistical findings and modulatory role of RUNX2 in cancer progression and provide biological information that can guide new research in this field.

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RUNX2 and LAMC2: promising pancreatic cancer biomarkers identified by an integrative data mining of pancreatic adenocarcinoma tissues

Cited by 10 publications

References 55 publications

S100A10 Promotes Pancreatic Ductal Adenocarcinoma Cells Proliferation, Migration and Adhesion through JNK/LAMB3-LAMC2 Axis

S100A10 Promotes Pancreatic Ductal Adenocarcinoma Cells Proliferation, Migration and Adhesion through JNK/LAMB3-LAMC2 Axis

Novel necroptosis-related gene signature for predicting the prognosis of pancreatic adenocarcinoma

RUNX2 and Cancer

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