C‐C motif chemokine ligand 23 abolishes ER stress‐ and LPS‐induced reduction in proliferation of bovine endometrial epithelial cells

Lim, Whasun; Bae, Hyocheol; Bazer, Fuller W.; Song, Gwonhwa

doi:10.1002/jcp.26210

Cited by 4 publications

(4 citation statements)

References 39 publications

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“…A bovine endometrial cell model showed that tunicamycin (an antibiotic)-induced ER stress inhibits epithelial cell proliferation ( 72 ). Addition of CCL23 rescued cell proliferation by activating PI3K/AKT and MAPK signaling while simultaneously reducing the expression levels of UPR-signaling proteins, including PERK, IRE1α, and ATF6.…”

Section: Ccl23-directed Er Stress Mitigationmentioning

confidence: 99%

CCL23 in Balancing the Act of Endoplasmic Reticulum Stress and Antitumor Immunity in Hepatocellular Carcinoma

Karan

2021

Front. Oncol.

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Endoplasmic reticulum (ER) stress is a cellular process in response to stress stimuli in protecting functional activities. However, sustained hyperactive ER stress influences tumor growth and development. Hepatocytes are enriched with ER and highly susceptible to ER perturbations and stress, which contribute to immunosuppression and the development of aggressive and drug-resistant hepatocellular carcinoma (HCC). ER stress-induced inflammation and tumor-derived chemokines influence the immune cell composition at the tumor site. Consequently, a decrease in the CCL23 chemokine in hepatic tumors is associated with poor survival of HCC patients and could be a mechanism hepatic tumor cells use to evade the immune system. This article describes the prospective role of CCL23 in alleviating ER stress and its impact on the HCC tumor microenvironment in promoting antitumor immunity. Moreover, approaches to reactivate CCL23 combined with immune checkpoint blockade or chemotherapy drugs may provide novel opportunities to target hepatocellular carcinoma.

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Section: Ccl23-directed Er Stress Mitigationmentioning

confidence: 99%

CCL23 in Balancing the Act of Endoplasmic Reticulum Stress and Antitumor Immunity in Hepatocellular Carcinoma

Karan

2021

Front. Oncol.

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“…In addition, a strong relationship between UPR and mTOR‐mediated autophagy has been reported in the literature (Gan et al, ; Rui, Xu, Chen, & Zhang, ). In addition, there is a growing number of reports of ER stress‐induced UPR and autophagy involved in female reproduction (Lim, Bae, Bazer, & Song, ; , ; Sobolewska et al, ; Tsukamoto et al, ). The results of this study indicate that COPS5 negatively regulates the ERN1 pathway and is positively correlated with the activity of mTOR‐autophagy signaling in this model.…”

Section: Discussionmentioning

confidence: 99%

COPS5 negatively regulates goat endometrial function via the ERN1 and mTOR‐autophagy pathways during early pregnancy

Yang

Zhang

Wang

et al. 2019

Journal Cellular Physiology

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In ruminant, adequate endometrial function is a major factor affecting implantation and economic efficiency. However, the precise mechanisms regulating goat endometrial function during the peri‐implantation period of pregnancy are still unclear. Here, we investigated the functional role and signal transduction of the fifth component of the constitutive photomorphogenic‐9 signalosome (COPS5) in the regulation of endometrial function in endometrial epithelial cells (EECs). Our results showed that hormones decreased COPS5 expression, and COPS5‐mediated regulation of endometrial function. We also found that knockdown of COPS5 hindered EECs proliferation by the G1‐phase cell cycle arrest. Hormones affected the activity of COPS5 through hormones receptors, while feedback from the expression of COPS5 regulated the transcription of the receptor. Moreover, knockdown of endoplasmic reticulum (ER) to nucleus signaling 1 (ERN1) via si‐ERN1 partly inhibited endometrial function in shCOPS5 EECs. In addition, blocking the mTOR pathway by rapamycin promoted endometrial function in si‐ERN1‐transfected shCOPS5 EECs. Overall, these results suggest that COPS5 negatively regulates goat endometrial function via the ERN1 and mTOR‐autophagy pathways and provide new insights into the mechanistic pathways of COPS5 during female reproductive development.

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“…In addition, CCL23 promotes the vascular endothelial growth factor (VEGF)-induced propagation and migration of endothelial cells [ 13 ]. Furthermore, CCL23 eliminates the endoplasmic reticulum stress and lipopolysaccharide-induced proliferation reduction in bovine endometrial epithelial cells [ 14 ]. In contrast, there are currently few studies indicating the involvement of CCL23 in cancer.…”

Section: Introductionmentioning

confidence: 99%

Inhibitory effect of CC chemokine ligand 23 (CCL23)/ transcription factor activating enhancer binding protein 4 (TFAP4) on cell proliferation, invasion and angiogenesis in hepatocellular carcinoma

Wang

Dai

et al. 2022

Bioengineered

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Hepatocellular carcinoma (HCC) is a highly vascularized solid tumor with a fast growth rate. According to bioinformatics analysis, CC chemokine ligand 23 (CCL23) has clinical significance for survival and prognosis in HCC. The online databases TCGA and CCLE were used to analyze the expression level of CCL23, and its expression was also measured in HCC cell lines by RT-qPCR and Western blotting. The STRING database and co-immunoprecipitation were employed to evaluate the association between CCL23 and transcription factor activating enhancer binding protein 4 (TFAP4). Overexpression plasmids for CCL23 (Ov-CCL23) and TFAP4 (Ov-TFAP4) were transfected into Huh-7 cells to detect TFAP4 expression. Huh-7 cells injected with OV-negative control (NC)/Ov-CCL23 or OV-NC/Ov-CCL23 plus Ov-TFAP4 were utilized to study the function of CCL23/TFAP4. Cell proliferation, invasion and human umbilical vein endothelial cell tube formation assays were conducted. The database revealed decreased expression of CCL23 in HCC and that it was commonly downregulated in HCC cell lines. TFAP4 expression was negatively correlated with CCL23. The overexpression of CCL23 inhibited the proliferation and invasion of Huh-7 cells, whereas TFAP4 blocked these effects. Similarly, the supernatant of CCL23-upregulated cells exhibited significantly lower tube formation potential, and low vascular endothelial growth factor A (VEGFA), VEGFRs expression compared with those of non-transfected Huh-7 cells, while TFAP4 plasmid co-transfected markedly increased these. Taken together, the present study suggests that CCL23 is expressed at low levels in HCC; it inhibits HCC cell proliferation, invasion and angiogenesis in vitro ; and its action is negatively associated with and can be blocked by TFAP4.

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C‐C motif chemokine ligand 23 abolishes ER stress‐ and LPS‐induced reduction in proliferation of bovine endometrial epithelial cells

Cited by 4 publications

References 39 publications

CCL23 in Balancing the Act of Endoplasmic Reticulum Stress and Antitumor Immunity in Hepatocellular Carcinoma

CCL23 in Balancing the Act of Endoplasmic Reticulum Stress and Antitumor Immunity in Hepatocellular Carcinoma

COPS5 negatively regulates goat endometrial function via the ERN1 and mTOR‐autophagy pathways during early pregnancy

Inhibitory effect of CC chemokine ligand 23 (CCL23)/ transcription factor activating enhancer binding protein 4 (TFAP4) on cell proliferation, invasion and angiogenesis in hepatocellular carcinoma

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