2021
DOI: 10.3389/fcell.2020.575903
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MICAL-L2 Is Essential for c-Myc Deubiquitination and Stability in Non-small Cell Lung Cancer Cells

Abstract: Objectives: MICAL-L2, a member of the molecules interacting with the CasL (MICAL) family, was reported to be highly expressed in several types of cancers, however, the roles of MICAL-L2 in NSCLC pathogenesis remain to be explored. This study is designed to clarify the mechanisms by which MICAL-L2 participates in NSCLC cell proliferation.Materials and Methods: The expression levels of MICAL-L2 in human lung cancer samples were assessed by immunohistochemical staining. Cells were transfected with siRNA or plasmi… Show more

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Cited by 11 publications
(11 citation statements)
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“…We also verified the high expression of MICALL2 in KIRC through GEPIA platform and GEO datasets. In accordance with the pan-cancer analysis, prior studies showed that MICALL2 is highly expressed in ovarian cancer, gastric cancer, and lung cancer demonstrated by western blot or immunohistochemical staining [17][18][19]. In addition, MICALL2 expressions increased with higher pathological grade, clinical stage, T classification, and M classification.…”
Section: Discussionsupporting
confidence: 64%
See 1 more Smart Citation
“…We also verified the high expression of MICALL2 in KIRC through GEPIA platform and GEO datasets. In accordance with the pan-cancer analysis, prior studies showed that MICALL2 is highly expressed in ovarian cancer, gastric cancer, and lung cancer demonstrated by western blot or immunohistochemical staining [17][18][19]. In addition, MICALL2 expressions increased with higher pathological grade, clinical stage, T classification, and M classification.…”
Section: Discussionsupporting
confidence: 64%
“…Gastric cancer cell migration is also potentiated through MICALL2 enhancing the stability of epidermal growth factor receptor (EGFR) [18]. In addition, MICALL2 binds to c-Myc and reduces its ubiquitin-dependent degradation, thus promoting the cell proliferation of non-small cell lung cancer (NSCLC) [19]. However, it remains poorly understood whether MICALL2 can be developed as an ideal biomarker to predict cancer progression and patient prognosis.…”
Section: Introductionmentioning
confidence: 99%
“…Similarly, MICAL2-induced ROS generation has also been reported to enhance the migratory potential of gastric cancer cells [ 34 ]. MICAL-L2 lacks the FAD domain and cannot generate ROS [ 35 ], and although several studies have suggested that MICAL-L2 may positively influence cancer progression [ 10 , 13 , 36 ], whether and how MICAL-L2 may be involved in this process remains unclear.…”
Section: Discussionmentioning
confidence: 99%
“…In ovarian cancer cells, the silencing of MICAL-L2 was shown to inhibit canonical Wnt/β-catenin signaling and induce mesenchymal–epithelial transition [ 11 ]. We have previously shown that MICAL-L2 facilitates the proliferation of lung cancer cells via the de-ubiquitination of c-Myc, which blocks its degradation [ 13 ]. Recently, another MICAL family member, MICAL1, which shares sequence similarity with MICAL-L2 [ 14 ], was found to play a key role in the migration and growth of colorectal cancer cells by suppressing the ERG1/β-catenin signaling pathway [ 15 ].…”
Section: Introductionmentioning
confidence: 99%
“…Members of the molecules interacting with the CasL ( MICAL ) gene family, including MICAL proteins and homologous MICAL-Like proteins, play important roles in diverse physiological processes [ 10 ]. MICAL can directly and specifically regulate actin dynamics, promoting semaphorin-induced signal conversion to promote F-actin instability-induced neuronal rejection [ 11 ].…”
Section: Introductionmentioning
confidence: 99%