Absence of CD74 Isoform at 41kDa Prevents the Heterotypic Associations between CD74 and CD44 in Human Lung Adenocarcinoma-derived Cells

Abdulmonem, Waleed Al; Rasheed, Zafar; Aljohani, Abdullah S. M.; Omran, Ola M.; Rasheed, Naila; Alkhamiss, Abdullah; Salloom, Abdulaziz A M Al; Alhumaydhi, Fahad A.; Alblihed, Mohamed A.; Ssadh, Hussain Al; Khan, Muhammad Ismail; Fernández, Nelson

doi:10.1080/08820139.2020.1790594

Cited by 7 publications

(5 citation statements)

References 28 publications

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“…Our data showed that after CD44 knockdown, the expression of CTSS in OS cells was consistent with the trend of MMP-9 and also showed downregulation. The regulation mechanism of CD44 in diseases has many crossed signalling pathways with CTSS, such as PI3K/AKT Pathway [49,50], P38 [51,52] and ERK1/2-MAPK signalling pathways [53,54], and other factors like MMP-9 and CD74 [55,56] are also involved. However, the exact regulatory relationship between the two has not been found in experimental studies.…”

Section: Discussionmentioning

confidence: 99%

Knockdown of CD44 inhibits proliferation, migration and invasion of osteosarcoma cells accompanied by downregulation of cathepsin S

Ji¹,

Gan

Cao

et al. 2022

J Orthop Surg Res

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Background Osteosarcoma (OS) is a malignant bone tumour of mesenchymal origin. These tumours are characterised by rich vascularisation, therefore promoting rapid proliferation and facilitating metastasis. CD44 has been reported to be involved in OS, but its role and molecular mechanisms in the pathogenesis of the disease are not fully determined. Methods In this study, we investigated the antitumor effect of CD44 on the development of OS and further explored the molecular mechanisms. The expression of CD44, cathepsin S and MMP-9 was detected by Western blot (WB) and reverse transcription-polymerase chain reaction (RT-qPCR) in different cell lines (MG63, U2OS OS and hFOB 1.19). To elucidate the role of CD44 in OS, MG63 and U2OS cells were treated with small interference RNA (siRNA) to knock down CD44, and the knockdown efficiency was validated with GFP and RT-qPCR. Furthermore, cell proliferation was assayed using Cell Counting Kit‑8 (CCK-8) and colony formation assays, and cell migration and invasion were assayed by transwell and wound-healing assays. Results We found that CD44 expression in the MG63 and U2OS OS cell lines was markedly increased compared to that of the human osteoblast hFOB 1.19 cell line. Knockdown of CD44 inhibited proliferation, migration and invasion of MG63 and U2OS cells. Cathepsin S expression in the MG63 and U2OS OS cell lines was increased compared to that of the human osteoblast hFOB 1.19 cell line. When CD44 was knocked down, its expression level went down. Conclusion Taken together, our data reinforced the evidence that CD44 knockdown inhibited cell proliferation, migration and invasion of OS cells accompanied by altered expression of cathepsin S. These findings offer new clues for OS development and progression, suggesting CD44 as a potential therapeutic target for OS.

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Section: Discussionmentioning

confidence: 99%

Knockdown of CD44 inhibits proliferation, migration and invasion of osteosarcoma cells accompanied by downregulation of cathepsin S

Ji¹,

Gan

Cao

et al. 2022

J Orthop Surg Res

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“…CD74 has been associated with cancer progression, 36 , 37 proinflammatory immune response, 38 has been implicated in regenerating tissues, 39 and is considered a monocytic/macrophagic marker within the myeloid branch of the hematopoietic system. Along with other cell types, differentiated cells of the hematopoietic system including macrophages and monocytes help create the BM niche in a healthy hematopoietic system, 34 supporting HSC survival and regulation.…”

Section: Discussionmentioning

confidence: 99%

Identification of cells of leukemic stem cell origin with non-canonical regenerative properties

Hollands,

Boyd,

Zhao

et al. 2024

Cell Reports Medicine

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“…To which extent the observed differences in CD74 isoform expression in microglia contribute to functional aspects remains unclear. Absence of the p41 CD74 isoform seems to prevent associations between CD74 and CD44 in human lung adenocarcinoma-derived cells [ 27 ]. Moreover, the invariant chain p41 mediates production of soluble MHC class II molecules [ 28 ].…”

Section: Discussionmentioning

confidence: 99%

Microglial CD74 Expression Is Regulated by TGFβ Signaling

Jahn

Bollensdorf

Kalischer

et al. 2022

IJMS

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Microglia play important roles during physiological and pathological situations in the CNS. Several reports have described the expression of Cd74 in disease-associated and aged microglia. Here, we demonstrated that TGFβ1 controled the expression of Cd74 in microglia in vitro and in vivo. Using BV2 cells, primary microglia cultures as well as Cx3cr1CreERT2:R26-YFP:Tgfbr2fl/fl in combination with qPCR, flow cytometry, and immunohistochemistry, we were able to provide evidence that TGFβ1 inhibited LPS-induced upregulation of Cd74 in microglia. Interestingly, TGFβ1 alone was able to mediate downregulation of CD74 in vitro. Moreover, silencing of TGFβ signaling in vivo resulted in marked upregulation of CD74, further underlining the importance of microglial TGFβ signaling during regulation of microglia activation. Taken together, our data indicated that CD74 is a marker for activated microglia and further demonstrated that microglial TGFβ signaling is important for regulation of Cd74 expression during microglia activation.

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Absence of CD74 Isoform at 41kDa Prevents the Heterotypic Associations between CD74 and CD44 in Human Lung Adenocarcinoma-derived Cells

Cited by 7 publications

References 28 publications

Knockdown of CD44 inhibits proliferation, migration and invasion of osteosarcoma cells accompanied by downregulation of cathepsin S

Knockdown of CD44 inhibits proliferation, migration and invasion of osteosarcoma cells accompanied by downregulation of cathepsin S

Identification of cells of leukemic stem cell origin with non-canonical regenerative properties

Microglial CD74 Expression Is Regulated by TGFβ Signaling

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