MiRNA-146a/AKT/β-Catenin Activation Regulates Cancer Stem Cell Phenotype in Oral Squamous Cell Carcinoma by Targeting CD24

Ghuwalewala, Sangeeta; Ghatak, Dishari; Das, Sumit; Roy, Stuti; Das, Pritha; Butti, Ramesh; Gorain, Mahadeo; Nath, Somsubhra; Kundu, Gopal C.; Roychoudhury, Susanta

doi:10.3389/fonc.2021.651692

Cited by 23 publications

(14 citation statements)

References 55 publications

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“…For example, Fu LC et.al showed that PD-L1 and β-catenin signaling make up a positive feedback loop to accelerate CSCs expansion and cancer progression by targeting putative stem cell marker LGR5 48 . The activation of miRNA-146a/AKT/β-catenin signaling promotes CSC phenotype in oral squamous cell carcinoma by regulating CD24, a classical maker of CSC 49 . Moreover, β-catenin mediates SOX2 induced-CSC phenotype, metastasis, and chemoresistance of CRC 50 .…”

Section: Discussionmentioning

confidence: 99%

METTL14 suppresses cancer stem cell phenotype of colorectal cancer via regulating of β-catenin/NANOG

Sun¹,

Chen²,

Xing³

et al. 2023

J. Cancer

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Cancer stem cell (CSC) characteristic contributes to tumor malignancy and progression. The role of N6-methyladenosine (m6A) modification in CSC characteristic is largely unknown. In this study, we found that m6A methyltransferase METTL14 was downregulated in colorectal cancer (CRC) and negatively correlated with the poor prognosis of CRC patients. Overexpression of METTL14 inhibited CSC characteristic, while knockdown of METTL14 promoted this characteristic. Through screening, NANOG was identified as the downstream of METTL14. Mechanically, we demonstrated that METTL14 inhibited cancer stem cell characteristic by regulating β-catenin. Collectively, our findings suggested that METTL16/β-catenin /NANOG axis might be promising therapeutic targets for CRC.

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Section: Discussionmentioning

confidence: 99%

METTL14 suppresses cancer stem cell phenotype of colorectal cancer via regulating of β-catenin/NANOG

Sun¹,

Chen²,

Xing³

et al. 2023

J. Cancer

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“…On the other hand, abnormally high expression of miR-146 was seen for the activation of CD24-AKT-β-catenin signaling, which significantly enhanced CSCs proliferation in vitro and tumorigenic ability in vivo [46].…”

Section: Non-melanoma Neoplastic Skin Disorders Squamous Cell Carcino...mentioning

confidence: 99%

miRNAs, Mesenchymal Stromal Cells and Major Neoplastic and Inflammatory Skin Diseases: A Page Being Written: A Systematic Review

Vincenzo

Diotallevi

Piccirillo

et al. 2023

IJMS

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Micro RNAs (miRNAs) are a type of non-coding RNA (ncRNA) and typically interact with specific target mRNAs through complementary base pairing, affecting their translation and/or stability. MiRNAs regulate nearly all cellular functions, including the cell fate of mesenchymal stromal cells (MSCs). It is now accepted that various pathologies arise at the stem level, and, in this scenario, the role played by miRNAs in the fate of MSCs becomes of primary concern. Here we have considered the existing literature in the field of miRNAs, MSCs and skin diseases, classified as inflammatory (such as psoriasis and atopic dermatitis-AD) and neoplastic (melanoma and non-melanoma-skin-cancer including squamous cell and basal cell carcinoma) diseases. In this scoping review article, the evidence recovered indicates that this topic has attracted attention, but it is still a matter of opinion. A protocol for this review was registered in PROSPERO with the registration number “CRD42023420245”. According to the different skin disorders and to the specific cellular mechanisms considered (cancer stem cells, extracellular vesicles, inflammation), miRNAs may play a pro- or anti-inflammatory, as well as a tumor suppressive, or supporting, role, indicating a complex regulation of their function. It is evident that the mode of action of miRNAs is more than a switch on–off, and all the observed effects of their dysregulated expression must be checked in a detailed analysis of the targeted proteins. The involvement of miRNAs has been studied mainly for squamous cell carcinoma and melanoma, and much less in psoriasis and AD; different mechanisms have been considered, such as miRNAs included in extracellular vesicles derived both from MSCs or tumor cells, miRNAs involved in cancer stem cells formation, up to miRNAs as candidates to be new therapeutic tools.

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“…CD24 is upregulated by HIF1α in human bladder cancer, 97 androgen receptor in urothelial carcinoma, 98 DNA methyltransferase, 99 estrogen receptor 100 and truncated glioma-associated oncogene homolog 1 101 in breast cancer. CD24 expression is negatively regulated by Twist in breast cancer, 102 β-catenin/TCF in colorectal cancer, 103 miR34a 104 and miR-146a 105 in oral squamous cell carcinoma, and histone deacetylase (HDAC) 99 in breast cancer. As a highly glycosylated GPI-anchored protein, the localization of CD24 on the membrane is regulated by the proteins related to both the synthesis of N and O sugars and GPI assembly, such as PIGN, PIGP, and PGAP2.…”

Section: Cd24mentioning

confidence: 99%

Emerging phagocytosis checkpoints in cancer immunotherapy

Liu

Wang

Yang

et al. 2023

Sig Transduct Target Ther

114

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Cancer immunotherapy, mainly including immune checkpoints-targeted therapy and the adoptive transfer of engineered immune cells, has revolutionized the oncology landscape as it utilizes patients’ own immune systems in combating the cancer cells. Cancer cells escape immune surveillance by hijacking the corresponding inhibitory pathways via overexpressing checkpoint genes. Phagocytosis checkpoints, such as CD47, CD24, MHC-I, PD-L1, STC-1 and GD2, have emerged as essential checkpoints for cancer immunotherapy by functioning as “don’t eat me” signals or interacting with “eat me” signals to suppress immune responses. Phagocytosis checkpoints link innate immunity and adaptive immunity in cancer immunotherapy. Genetic ablation of these phagocytosis checkpoints, as well as blockade of their signaling pathways, robustly augments phagocytosis and reduces tumor size. Among all phagocytosis checkpoints, CD47 is the most thoroughly studied and has emerged as a rising star among targets for cancer treatment. CD47-targeting antibodies and inhibitors have been investigated in various preclinical and clinical trials. However, anemia and thrombocytopenia appear to be formidable challenges since CD47 is ubiquitously expressed on erythrocytes. Here, we review the reported phagocytosis checkpoints by discussing their mechanisms and functions in cancer immunotherapy, highlight clinical progress in targeting these checkpoints and discuss challenges and potential solutions to smooth the way for combination immunotherapeutic strategies that involve both innate and adaptive immune responses.

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MiRNA-146a/AKT/β-Catenin Activation Regulates Cancer Stem Cell Phenotype in Oral Squamous Cell Carcinoma by Targeting CD24

Cited by 23 publications

References 55 publications

METTL14 suppresses cancer stem cell phenotype of colorectal cancer via regulating of β-catenin/NANOG

METTL14 suppresses cancer stem cell phenotype of colorectal cancer via regulating of β-catenin/NANOG

miRNAs, Mesenchymal Stromal Cells and Major Neoplastic and Inflammatory Skin Diseases: A Page Being Written: A Systematic Review

Emerging phagocytosis checkpoints in cancer immunotherapy

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