Overexpression of Copines‐1 is associated with clinicopathological parameters and poor outcome in gastric cancer

Yang, Jun; Wang, Yingjing; Ge, Rong; Jia, Xiupeng; Ge, Congshan; Cen, Youqing; Pan, Deng

doi:10.1002/jcla.24744

Cited by 3 publications

(1 citation statement)

References 29 publications

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“…There is still much need for improvement in the current therapeutic approaches for gastric cancer, including surgery, neoadjuvant radiotherapy, molecular targeted therapy, and immunotherapy. Despite these treatment options, the outcomes for advanced forms of the disease are not satisfactory (Yang et al, 2022). With this in mind, it becomes crucial to unearth groundbreaking biomarkers that can aid in the early detection of the disease and ultimately enhance the clinical outlook for patients diagnosed with STAD.…”

Section: Introductionmentioning

confidence: 99%

CLCA1 is Poorly Expressed in Stomach Adenocarcinoma and Correlates with Immune Infiltration

Zhao,

Chen,

et al. 2024

Int. J. Morphol.

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Calcium-activated chloride channel regulator 1 (CLCA1) is associated with cancer progression. The expression and immunologic function of CLCA1 in stomach adenocarcinoma (STAD) remain unclear. In this investigation, the expression of CLCA1 in STAD tissues and its involvement in the progression and immune response of STAD were examined using databases such as cBioPortal, TISIDB, and UALCAN. In order to validate the expression level of CLCA1 protein in gastric adenocarcinoma, thirty clinical tissue specimens were gathered for immunohistochemical staining. The findings indicated a downregulation of CLCA1 in STAD patients, which was correlated with race, age, cancer grade, Helicobacter pylori infection, and molecular subtype. Through the examination of survival analysis, it was identified that diminished levels of CLCA1 within gastric cancer cases were linked to decreased periods of post-progression survival (PPS), overall survival (OS), and first progression (FP) (P<0.05). The CLCA1 mutation rate was lower in STAD, but the survival rate was higher in the variant group. The correlation between the expression level of CLCA1 and the levels of immune infiltrating cells in STAD, as well as the immune activating molecules, immunosuppressive molecules, MHC molecules, chemokines, and their receptor molecules, was observed. Gene enrichment analysis revealed that CLCA1 may be involved in STAD progression through systemic lupus erythematosus (SLE), proteasome, cell cycle, pancreatic secretion, and PPAR signaling pathways. In summary, CLCA1 is anticipated to function as a prognostic marker for patients with STAD and is linked to the immunization of STAD.

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Section: Introductionmentioning

confidence: 99%

CLCA1 is Poorly Expressed in Stomach Adenocarcinoma and Correlates with Immune Infiltration

Zhao,

Chen,

et al. 2024

Int. J. Morphol.

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Role of CPNE1 in Odontoblastic Differentiation of Rat Stem Cells from Apical Papilla

Xie

et al. 2023

Advanced Biology

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CPNE1 is a calcium‐dependent, phospholipid‐binding protein that is ubiquitously expressed in various tissues and organs. This study investigates the expression and localization of CPNE1 in tooth germ development and the role of CPNE1 in odontoblastic differentiation. In rat tooth germs, CPNE1 is expressed in the odontoblasts and ameloblasts since the late bell stage. The depletion of CPNE1 in the stem cells from apical papilla (SCAPs) clearly inhibits the expression of odontoblastic‐related genes and the formation of mineralized nodules during differentiation, while CPNE1 overexpression promotes this process. In addition, CPNE1 overexpression increases AKT phosphorylation during the odontoblastic differentiation of SCAPs. Furthermore, treatment with AKT inhibitor (MK2206) reduces the expression of odontoblastic‐related genes in CPNE1 over‐expressed SCAPs, and Alizarin Red staining shows reduced mineralization. These results suggest that CPNE1 plays a role in the tooth germ development as well as the odontblastic differentiation of SCAPs in vitro that is related to the AKT signaling pathway.

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