SFMBT2-Mediated Infiltration of Preadipocytes and TAMs in Prostate Cancer

Gwak, Jungsug; Jeong, Hayan; Lee, Sang Hoon; Shin, Jee Yoon; Sim, Taejun; Na, Jungtae; Kim, Jongchan

doi:10.3390/cancers12092718

Cited by 10 publications

(12 citation statements)

References 103 publications

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“…To identify the circRNAs that could sponge miR-491 in CRC, circBase and starBase databases were used to identify potential circRNAs, that could bind to and sponge miR-491 ( Table SII ). As SFMBT2 is widely involved in cancer processes ( 20 , 21 ), from the results, hsa-circ-0000212 was selected, which is derived from the SFMBT2 gene (chromosome 10, 7405839-7423911). The expression levels of circ-0000212 were assessed in the CRC cell lines, and it was found that circ-0000212 was notably increased when compared with that in the normal FHC cell line, although the difference was not significant ( Fig.…”

Section: Resultsmentioning

confidence: 99%

circ‑0000212 promotes cell proliferation of colorectal cancer by sponging miR‑491 and modulating FOXP4 expression

Tao

Zhang

et al. 2021

Mol Med Rep

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Colorectal cancer (CRC) is a lethal and common malignancy worldwide. Non-coding (nc)RNAs have been shown to modulate tumor progression in several types of cancer. The present study aimed to investigate the role of hsa_circ_0000212 in CRC, as a sponge of microRNA (miR)-491. The expression levels of miR-491 and forkhead box P4 (FOXP4) were analyzed using data from The Cancer Genome Atlas. The association between miR-491 and FOXP4 and the clinicopathological characteristics were also analyzed. A novel circular (circ)RNA, hsa_circ_0000212, was found to sponge miR-491 based on bioinformatics analysis. The potential binding site between miR-491 and FOXP4 or circ-0000212 was validated using luciferase and RNA immunoprecipitation assays. The expression levels and distribution of circ-0000212 was also determined. Cell Counting Kit-8 and colony formation assays were performed to determine the role of miR-491 or circ-0000212 on the proliferation of the CRC cells. Decreased miR-491 or increased FOXP4 expression levels were associated with the pathological stage in patients with CRC. In addition, miR-491 inhibited cell proliferation by targeting FOXP4. circ-0000212 was increased in CRC tissues and was predominantly localized in the cytoplasm. Furthermore, circ-0000212 augmented viability of the CRC cells by sponging miR-491 and modulating FOXP4. In conclusion, circ-0000212 may serve as a novel tumor-promoter and drug target in CRC.

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Section: Resultsmentioning

confidence: 99%

circ‑0000212 promotes cell proliferation of colorectal cancer by sponging miR‑491 and modulating FOXP4 expression

Tao

Zhang

et al. 2021

Mol Med Rep

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“…CXCL10 is a notable cytokine, which has been found in elevated levels in both cancer and COVID-19 patients, driving metastasis, inflammation and poor clinical outcomes in both the cases [55,56]. A study by Gwak et al [57] on the prostate cancer microenvironment found that multiple inflammatory cytokines including CXCL10 were upregulated in PRAD patients. CXCL10 plays a significant role in the tumor metastasis and immunesuppression in prostate cancer and being a tumor-associated macrophage, it also promotes tumor microenvironment creation, migration and invasion of prostate cancer cells [37][38][39].…”

Section: Discussionmentioning

confidence: 99%

“…IL-1β, IL-6, CXCL8, CXCL10, and vascular endothelial growth factor comprise the M2 TAMs that contribute to cancer metastasis, immune suppression, and tumor growth. Moreover, elevated levels of CXCL8, CCL2, CXCL10, and CCL20 have been found in prostate cancer patients with Gleason score ≥ 8 [ 57 ]. Again, COVID-19 patients too have upregulated levels of inflammatory cytokines which makes the disease prognosis critical in patients.…”

Section: Discussionmentioning

confidence: 99%

A systemic study on the vulnerability and fatality of prostate cancer patients towards COVID-19 through analysis of the TMPRSS2, CXCL10 and their co-expressed genes

Raza¹,

Mizan²

2022

Genomics Inform

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A pandemic of respiratory disease named coronavirus disease 2019 (COVID-19) is caused by a novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). It is reported prostate cancer patients are susceptible to COVID-19 infection. To understand the possible causes of prostate cancer patients' increased vulnerability and mortality from COVID-19 infection, we focused on the two most important agents, transmembrane protease serine subtype 2 (TMPRSS2) and the C-X-C motif 10 (CXCL10). When SARS-CoV-2 binds to the host cell via S protein–angiotensin-converting enzyme-2 receptor interaction, TMPRSS2 contributes in the proteolytic cleavage of the S protein, allowing the viral and cellular membranes to fuse. CXCL10 is a cytokine found in elevated level in both COVID-19 and cancer-causing cytokine storm. We discovered that TMPRSS2 and CXCL10 are overexpressed in prostate cancer and COVID-19 using the UALCAN and GEPIA2 datasets. The functional importance of TMPRSS2 and CXCL10 in prostate cancer development was then determined by analyzing the frequency of genetic changes in their amino acid sequences using the cBioPortal online portal. Finally, we used the PANTHER database to examine the pathology of the targeted genes. We observed that TMPRSS2 and CXCL10, together with their often co-expressed genes, are important in the binding activity and immune responses in prostate cancer and COVID-19 infection, respectively. Finally, we found that TMPRSS2 and CXCL10 are two putative biomarkers responsible for the increased vulnerability and fatality of prostate cancer patients to COVID-19.

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“…STAT3 transcriptionally inhibited the tumor suppressor miR-506-3p in CRC cells ( Wei et al, 2019 ). It was also shown in another study that IL-6 secreted by TAMs promote the invasion of the prostate cancer cells and express low levels of the epigenetic factor (SFMBT2) ( Gwak et al, 2020 ).…”

Section: Introductionmentioning

confidence: 93%

A cutting-edge immunomodulatory interlinkage between HOTAIR and MALAT1 in tumor-associated macrophages in breast cancer: A personalized immunotherapeutic approach

Amer

Eissa²,

Tayebi³

2022

Front. Mol. Biosci.

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Breast cancer (BC) is one of the most common cancers, accounting for 2.3 million cases worldwide. BC can be molecularly subclassified into luminal A, luminal B HER2-, luminal B HER2+, HER2+, and triple-negative breast cancer (TNBC). These molecular subtypes differ in their prognosis and treatment strategies; thus, understanding the tumor microenvironment (TME) of BC could lead to new potential treatment strategies. The TME hosts a population of cells that act as antitumorigenic such as tumor-associated eosinophils or pro-tumorigenic such as cancer-associated fibroblasts (CAFs), tumor-associated neutrophils (TANs), monocytic-derived populations such as MDSCs, or most importantly “tumor-associated macrophages (TAMs),” which are derived from CD14+ monocytes. TAMs are reported to have the pro-inflammatory phenotype M1, which is found only in the very early stages of tumor and is not correlated with progression; however, the M2 phenotype is anti-inflammatory that is correlated with tumor progression and metastasis. The current study focused on controlling the anti-inflammatory activity in TAMs of hormonal, HER2+, and TNBC by epigenetic fine-tuning of two immunomodulatory proteins, namely, CD80 and mesothelin (MSLN), which are known to be overexpressed in BC with pro-tumorigenic activity. Long non-coding RNAs are crucial key players in tumor progression whether acting as oncogenic or tumor suppressors. We focused on the regulatory role of MALAT1 and HOTAIR lncRNAs and their role in controlling the tumorigenic activity of TAMs. This study observed the impact of manipulation of MALAT1 and HOTAIR on the expression of both CD80 and MSLN in TAMs of BC. Moreover, we analyzed the interlinkage between HOTAIR and MALAT1 as regulators to one another in TAMs of BC. The current study reported an upstream regulatory effect of HOTAIR on MALAT1. Moreover, our results showed a promising use of MALAT1 and HOTAIR in regulating oncogenic immune-modulatory proteins MSLN and CD80 in TAMs of HER2+ and TNBC. The downregulation of MALAT1 and HOTAIR resulted in the upregulation of CD80 and MSLN, which indicates that they might have a cell-specific activity in TAMs. These data shed light on novel key players affecting the anti-inflammatory activity of TAMs as a possible therapeutic target in HER2+ and TNBC.

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SFMBT2-Mediated Infiltration of Preadipocytes and TAMs in Prostate Cancer

Cited by 10 publications

References 103 publications

circ‑0000212 promotes cell proliferation of colorectal cancer by sponging miR‑491 and modulating FOXP4 expression

circ‑0000212 promotes cell proliferation of colorectal cancer by sponging miR‑491 and modulating FOXP4 expression

A systemic study on the vulnerability and fatality of prostate cancer patients towards COVID-19 through analysis of the TMPRSS2, CXCL10 and their co-expressed genes

A cutting-edge immunomodulatory interlinkage between HOTAIR and MALAT1 in tumor-associated macrophages in breast cancer: A personalized immunotherapeutic approach

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