C5aR1 promotes the progression of colorectal cancer by EMT and activating Wnt/β-catenin pathway

Xu, Duo; Li, Meirong; Ran, Longyan; Li, Xiaochen; Sun, Xingwang; Yin, Tao

doi:10.1007/s12094-022-02956-y

Cited by 10 publications

(5 citation statements)

References 35 publications

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“…Another candidate marker, C5AR1, is expressed in both myeloid cells and non-myeloid cells [36] and has been associated with increased recruitment and polarisation of macrophages to an M2 state in CRCLM and pancreatic cancer LM [29,[36][37][38]. The expression of TTYH3, another identified marker, has been associated with poor prognosis and poor response to immunotherapy in lung cancer [39] with high level of expression associated with immune cell infiltration, specifically macrophages and T-reg cells [39][40][41][42][43][44][45][46][47][48].…”

Section: Discussionmentioning

confidence: 99%

Circulating extracellular vesicles containing S100A9 reflect histopathology, immunophenotype and therapeutic responses of liver metastasis in colorectal cancer patients

Tsamchoe

Lazaris

Kim

et al. 2023

BJC Rep

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Background Metastasis is the principal cause of cancer treatment failure and an area of dire diagnostic needs. Colorectal cancer metastases to the liver (CRCLMs) are predominantly classified into desmoplastic and replacement based on their histological growth patterns (HGPs). Desmoplastic responds well to current treatments, while replacement HGP has a poor prognosis with low overall survival rates. Methods We hypothesised that complex cellular response underlying HGPs may be reflected in the proteome of circulating extracellular vesicles (EVs). EV proteomics data was generated through LC-MS/MS and analysed with Maxquant and Perseus. To validate the S100A9 signature, ELISA was performed, and IHC and IF were conducted on tissue for marker detection and colocalization study. Results Plasma EV proteome signature distinguished desmoplastic from the replacement in patients with 22 differentially expressed proteins, including immune related markers. Unsupervised PCA analysis revealed clear separation of the two lesions. The marker with the highest confidence level to stratify the two HGPs was S100A9, which was traced in CRCLM lesions and found to colocalize with macrophages and neutrophils. EV-associated S100A9 in plasma may reflect the innate immunity status of metastatic lesions and their differential therapeutic responses. Conclusion Plasma EV-derived S100A9 could be useful in personalising therapy in patients with CRCLM.

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Section: Discussionmentioning

confidence: 99%

Circulating extracellular vesicles containing S100A9 reflect histopathology, immunophenotype and therapeutic responses of liver metastasis in colorectal cancer patients

Tsamchoe

Lazaris

Kim

et al. 2023

BJC Rep

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“…Previous study, we performed RNA-seq with SETDB1 stable knockdown and overexpression cell line HCT116 by Biomarker Technology Corporation (Beijing, China) with log2|fold change|≥ 1.5 and P-value < 0.05 32 . As more DEGs were fund in SETDB1 kncokdown cells.…”

Section: Rna-seqmentioning

confidence: 99%

“…Human CRC cell lines SW620, HCT116, SW480 used in this study were self-stored in the Department of Pathology, Affiliated Hospital of Southwest Medical University. The origin and cultural conditions were described before 32 . Using Lipofectamine 2000, cells were transfected with ADORA2A siRNA or ADORA2A overexpressed plastic after cell density reached around 50%.…”

Section: Cell Culture and Transfectionmentioning

confidence: 99%

ADORA2A promotes proliferation and inhibits apoptosis through PI3K/AKT pathway activation in colorectal carcinoma

Ran,

Mou,

Peng

et al. 2023

Sci Rep

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The third most often diagnosed disease globally and the second most prevalent cause of cancer-related death is colorectal cancer (CRC). Numerous human malignancies have been identified to have high expression of ADORA2A. However, it is still ambiguous about its function in CRC. RNA-seq with stable transfected SETDB1 knockdown cells was used to identify differentially expressed genes. Further, knockdown of ADORA2A in CRC cell lines SW620 and HCT116 was performed with siRNA and over expression of ADORA2A in SW480 cells was conducted with plasmids. CCK8, colony formation, wound healing, and transwell assay were used to detect the effects of cell proliferation, migration, and invasion after knockdown and over expression of ADORA2A. Also, apoptosis was analyzed by flow cytometry, apoptosis-related proteins and key PI3K/AKT pathway proteins were detected using Western blotting. ADORA2A was identified after RNA-seq analysis and played an important role in CRC prognosis. ADORA2A was relatively high in SW620 and HCT116 cell lines compared to SW480 cell lines. ADORA2A knockdown in SW620 and HCT116 inhibited cell proliferation, migration, and invasion, while ADORA2A overexpression had the opposite effect. In addition, ADORA2A also impacted the expression of apoptosis-related proteins, including Bcl-2, Bax, Cleaved caspase-3 and Cleaved caspase-9, and reduced apoptosis. Furthermore, this process may include the PI3K/AKT signaling pathway. ADORA2A promotes CRC progression and inhibits apoptosis by the PI3K/AKT signaling pathway. It may contribute to the management and treatment of CRC.

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“…Human CRC cell lines used in this study were SW620, HCT116 and SW480. The origin and culture conditions were described before [9]. Using Lipofectamine 2000, the cells were transfected with ADORA2A siRNA or ADORA2A overexpressed plastic after the cell density reached around 50%.…”

Section: Cell Culture and Transfectionmentioning

confidence: 99%

“…RNA-seq was performed with SETDB1 stable knockdown cell line SW620 by Biomarker Technology Corporation (Beijing, China) as previous described with log2|fold change| ≥ 1.5 and P-value < 0.05 [9].…”

Section: Rna-seqmentioning

confidence: 99%

ADORA2A promotes proliferation and inhibits apoptosis through PI3K/AKT pathway activation in colorectal carcinoma

Ran

Mou

Peng

et al. 2022

Preprint

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Background：The third most often diagnosed disease globally and the second most prevalent cause of cancer-related death is colorectal cancer (CRC). Numerous human malignancies have been identified to overexpress ADORA2A. However, it is still ambiguous about its function in CRC. Methods: RNA-seq with stable transfected SETDB1 knockdown cells was used to identify the differentially expressed genes. Further, knockdown of ADORA2A in CRC cell lines SW620 and HCT116 were performed with siRNA and overexpression of ADORA2A in SW480 cells were conducted with plasmid. CCK8, colony formation, wound healing and transwell assay were used to detect the effects of cell proliferation, migration and invasion after knockdown and overexpression of ADORA2A. Also, apoptosis was analyzed by flow cytometry, apoptosis-related proteins and key PI3K/AKT pathway proteins were detected using western blotting. Results: ADORA2A was obtained with RNA-seq and played an important role in CRC prognosis. ADORA2A was relatively high expressed in SW620 and HCT116 cell lines compared to SW480 cell line. Knockdown of ADORA2A in SW620 and HCT116 cell lines inhibited cell proliferation, migration and invasion while overexpression of ADORA2A had the opposite results. In addition, ADORA2A also impacted the expression of apoptosis-related proteins, including as Bcl-2, Bax, caspase3 and caspase9, and reduced apoptosis. Furthermore, this process may include the PI3K/AKT signal pathway. Conclusion: ADORA2A promotes CRC progression by PI3K/AKT signaling pathway. It might contribute to management and treatment of CRC.

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C5aR1 promotes the progression of colorectal cancer by EMT and activating Wnt/β-catenin pathway

Cited by 10 publications

References 35 publications

Circulating extracellular vesicles containing S100A9 reflect histopathology, immunophenotype and therapeutic responses of liver metastasis in colorectal cancer patients

Circulating extracellular vesicles containing S100A9 reflect histopathology, immunophenotype and therapeutic responses of liver metastasis in colorectal cancer patients

ADORA2A promotes proliferation and inhibits apoptosis through PI3K/AKT pathway activation in colorectal carcinoma

ADORA2A promotes proliferation and inhibits apoptosis through PI3K/AKT pathway activation in colorectal carcinoma

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