Complex mixtures of pesticides and metabolites modulate the malignant phenotype of murine melanoma B16-F1 cells

Roque, Aliciane de Almeida; Luz, Jessica Zablocki da; Santurio, Michelle Thays Khun; Neto, Francisco Filipak; Ribeiro, Ciro Alberto de Oliveira

doi:10.1007/s11356-023-25603-7

Cited by 4 publications

(1 citation statement)

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“…Prior to cancer cell metastasis, the primary tumor releases certain factors, including extracellular matrix (ECM) structural proteins that actively stimulate the metastatic site, while MMP14 plays a regulatory role in the ECM remodeling process [51]. In studies on melanoma, MMP14 is a regulatory factor for invasion [52], and the invasiveness of melanoma cells can be decreased by inhibiting MMP14 [53]. The MMP14 knockdown model in mice illustrated normal development and reproduction but reduced growth and metastasis of melanoma, and decreased vascular permeability [54], this indicates that MMP14 is a pivotal factor in melanoma progression.…”

Section: Discussionmentioning

confidence: 99%

Calreticulin regulates the expression of MMP14 and ADAR1 through EIF2AK2 signaling to promote the proliferation and progression of malignant melanoma cells

Liang,

Wang,

Guo

et al. 2024

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It has been demonstrated that calreticulin (CALR) is expressed abnormally in various tumors and is involved in the occurrence and development of tumors. In this study, CALR and EIF2AK2 expression was measured in the clinical specimens of 39 patients with melanoma. Then, we constructed knockdown and overexpression cell models of CALR and EIF2AK2 and used wound healing and Transwell assays to observe cell migration and invasion. Apoptosis, EDU, and ROS assays were used to measure cell apoptosis and proliferation, as well as ROS levels. The effect of CALR on endoplasmic reticulum stress was detected using endoplasmic reticulum fluorescent probes. Western blotting was used to detect protein levels of CALR, EIF2AK2, ADAR1, and MMP14. The results indicated that CALR and EIF2AK2 expression levels were significantly higher in human melanoma tissues than in adjacent non-tumor tissue. In addition, we found a correlation between CALR and the expression of EIF2AK2 and MMP14, and the experimental results indicated that overexpression of CALR significantly upregulated the expression of EIF2AK2, MMP14, and ADAR1, while knockdown of CALR inhibited their expression. Notably, the knockdown of EIF2AK2 in the CALR overexpression group blocked the upregulation of MMP14 and ADAR1 expression by CALR, and the knockdown of both CALR and EIF2AK2 significantly inhibited MMP14 and ADAR1 expression. In conclusion, CALR and EIF2AK2 play a promoting role in melanoma progression, and knockdown of CALR and EIF2AK2 may be an effective anti-tumor target, and its mechanism may be through MMP14, ADAR1 signaling.

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