Interferon induced transmembrane protein 3 regulates the growth and invasion of human lung adenocarcinoma

Dong, Zehua; Wang, Huimin; He, Huijie; Niu, Haiying; Yu, Li

doi:10.1111/1759-7714.12451

Cited by 31 publications

(25 citation statements)

References 27 publications

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“…In gastric carcinoma cell lines, knockdown of IFITM3 significantly suppresses tumor cell migration, invasion and proliferation in vitro ( 24 ). Similar results are observed in colonic ( 23 ), breast ( 25 ), prostate ( 26 ), liver ( 28 ), glioma ( 21 ), and lung cancer cell lines ( 27 ). IFITM3 knock out tumor cells (IFITM3 -/- ) arrest at the G0/G1 phase and many cancer cell types display a reduced number of cells in the S phase ( 21 , 23 – 25 , 28 ).…”

Section: Ifitm3 Expression In Cancersupporting

confidence: 75%

“…Early work suggested IFITM3 is a cancer biomarker, following observed overexpression in colonic cancers and gliomas (20,21). Subsequently, IFITM3 overexpression in cancer tissues as compared to healthy adjacent tissue was confirmed in other cancers, including colonic (22,23), gastric (24), breast (25), prostate (26), lung (27), and liver (28) (Figures 1B, C). IFITM3 expression is higher in metastatic lymph nodes and bone metastases when compared to primary tumors (23,26).…”

Section: Ifitm3 Expression In Cancer the Relationship Between Ifitm3 mentioning

confidence: 83%

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Malignancy and IFITM3: Friend or Foe?

2020

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The prevalence and incidence of cancers has risen over the last decade. Available treatments have improved outcomes, yet mortality and morbidity remain high, creating an urgent demand for personalized and new therapy targets. Interferon induced transmembrane protein (IFITM3) is highly expressed in cancers and is a marker of poor prognosis. In this review, we discuss recent advances in IFITM3 biology, the regulatory pathways, and its function within cancer as part of immunity and maintaining stemness. Overexpression of IFITM3 is likely an indirect effect of ongoing inflammation, immune and cancer epithelial-to-mesenchymal (EMT) related pathways i.e., interferons, TGF-β, WNT/β-catenin, etc. However, IFITM3 also influences tumorigenic phenotypes, such as cell proliferation, migration and invasion. Furthermore, IFITM3 plays a key role in cancer growth and maintenance. Silencing of IFITM3 reduces these phenotypes. Therefore, targeting of IFITM3 will likely have implications for potential cancer therapies.

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Section: Ifitm3 Expression In Cancersupporting

confidence: 75%

Section: Ifitm3 Expression In Cancer the Relationship Between Ifitm3 mentioning

confidence: 83%

Malignancy and IFITM3: Friend or Foe?

2020

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“…The M5-T1 tumor was also specifically characterized by important changes in the content of several transmembrane proteins and components of the extracellular matrix. Among proteins belonging to the first category, IFM3 was reported to be highly expressed in invasive phenotypes of different types of cancer [ 61 , 62 ]. CSPG4, a cell surface proteoglycan, was overexpressed in a huge range of human and animal tumors, the tumor microenvironment, and cancer initiating cells [ 63 ].…”

Section: Discussionmentioning

confidence: 99%

Characterization of increasing stages of invasiveness identifies stromal/cancer cell crosstalk in rat models of mesothelioma

et al. 2018

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Sarcomatoid mesothelioma (SM) is a devastating cancer associated with one of the poorest outcome. Therefore, representative preclinical models reproducing different tumor microenvironments (TME) observed in patients would open up new prospects for the identification of markers and evaluation of innovative therapies. Histological analyses of four original models of rat SM revealed their increasing infiltrative and metastatic potential were associated with differences in Ki67 index, blood-vessel density, and T-lymphocyte and macrophage infiltration. In comparison with the noninvasive tumor M5-T2, proteomic analysis demonstrated the three invasive tumors F4-T2, F5-T1 and M5-T1 shared in common a very significant increase in the abundance of the multifunctional proteins galectin-3, prohibitin and annexin A5, and a decrease in proteins involved in cell adhesion, tumor suppression, or epithelial differentiation. The increased metastatic potential of the F5-T1 tumor, relative to F4-T2, was associated with an increased macrophage vs T-cell infiltrate, changes in the levels of expression of a panel of cytokine genes, an increased content of proteins involved in chromatin organization, ribosome structure, splicing, or presenting anti-adhesive properties, and a decreased content of proteins involved in protection against oxidative stress, normoxia and intracellular trafficking. The most invasive tumor, M5-T1, was characterized by a pattern of specific phenotypic and molecular features affecting the presentation of MHC class I-mediated antigens and immune cell infiltration, or involved in the reorganization of the cytoskeleton and composition of the extracellular matrix. These four preclinical models and data represent a new resource available to the cancer research community to catalyze further investigations on invasiveness.

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“…However, IFITM expression abnormalities have been observed in various cancers, and IFITM gene disruption has been associated with tumor malignancy and growth. 31,83,84 The differing trafficking strategy used by VSV-G pseudotyped LVs, compared with HIV-1, exposes LV to distinct restriction factors that may affect integration and alter latency. 29,35 Thus, an open question is whether transient pharmacologic IFITM modulation is a genetically safe approach.…”

Section: Discussionmentioning

confidence: 99%