Serum FBLN1 and STK31 as biomarkers of colorectal cancer and their ability to noninvasively differentiate colorectal cancer from benign polyps

Watany, Mona Mohamed; Elmashad, Nehal; Badawi, Rehab; Hawash, Nehad

doi:10.1016/j.cca.2018.04.038

Cited by 18 publications

(11 citation statements)

References 18 publications

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“…Plasma fibulin-1 level is significantly increased in plasma of patients with HCC compared with those in healthy controls, individuals with chronic hepatitis B, and patients with HBV-induced liver cirrhosis [159]. A similar situation was observed in the case of CRC and malignant mesothelioma [160][161][162]. Fibulin-1 and cathepsin F (CTSF) levels were specifically upregulated in sera and tissues of patients with NSCLC with brain metastasis (BM) compared with NSCLC without BM and primary brain tumor.…”

Section: Fibulin-1 (Fbln1_human)supporting

confidence: 54%

Construction of 2DE-Patterns of Plasma Proteins: Aspect of Potential Tumor Markers

Naryzhny¹,

Ронжина²,

Zorina³

et al. 2022

Preprint

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Cancer is a complex systemic disease that changes the entire proteome. The analysis of this transformation makes it possible to determine tumor markers, that is, the most characteristic biomacromolecules produced by tumor cells. Here, the question of finding ideal tumor markers, which should be sensitive, specific, and reliable, is an acute issue. Unfortunately, none of the tumor markers, even those used in the clinic, has all these characteristics. Despite this, many tumor markers have demonstrated excellent clinical relevance for monitoring the effectiveness of different treatments for cancer patients. The use of markers also aids in the early detection of cancer recurrence and prognosis. Therefore, the situation in this area can be improved in two ways – by attempting to find an ideal single tumor marker or generating panels of different markers. In both cases, proteomics certainly plays a major role. Human plasma is one of the most popular samples as it is commonly collected in the clinic and provides noninvasive, rapid analysis for any type of disease including cancer. Many efforts have been applied in searching for “ideal” tumor markers digging very deep plasma proteome. There is a line of evidence that the most abundant, so-called “classical plasma proteins”, may be used to generate a tumor biomarker profile. To be comprehensive these profiles should have information not only about protein levels but proteoform distribution for each protein. Initially, the profile of these proteins in norm should be generated. Here, we present data about these profiles generated by two-dimensional electrophoresis with the following mass-spectrometry and immunodetection.

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Section: Fibulin-1 (Fbln1_human)supporting

confidence: 54%

Construction of 2DE-Patterns of Plasma Proteins: Aspect of Potential Tumor Markers

Naryzhny¹,

Ронжина²,

Zorina³

et al. 2022

Preprint

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“…to contribute to the tumorigenicity of epithelial cancer, and overexpression of STK31 promoted cell migration and invasion, whereas STK31 knockdown induced apoptosis (17). In addition, STK31 has been revealed to be a novel biomarker for the risk of colorectal cancer metastasis (19,20). However, the roles and underlying mechanisms of STK31 in lung cancer cells remain unclear.…”

Section: Stk31 Regulates the Proliferation And Cell Cycle Of Lung Canmentioning

confidence: 99%

STK31 regulates the proliferation and cell cycle of lung cancer cells via the Wnt/β‑catenin pathway and feedback regulation by c‑myc

Xiong¹,

Xing²,

Zheng³

et al. 2019

Oncol Rep

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Lung cancer, which is a leading cause of cancer-related deaths, is diagnosed at a male to female ratio of 2.1:1. Serine-threonine kinase 31 (STK31) is a novel cancer/testis (CT)-related gene that is highly expressed in several types of cancers, such as lung and colorectal cancer, and plays crucial roles in cancer. In the present study, increased expression of STK31 and β-catenin was observed in lung cancer tissues and cell lines. Downregulation of STK31 expression in lung cancer cells significantly inhibited their proliferation by arresting the cell cycle in the G1 phase concurrent with decreased β-catenin, c-myc and cyclin D1 protein levels, while upregulation of STK31 had the opposite effects. In addition, STK31-induced lung cancer cell viability, proliferation, cell cycle progression, and expression of related genes were completely attenuated by a Wnt/β-catenin inhibitor (XAV939). Similar to XAV939, a c-myc inhibitor (10058-F4) also significantly attenuated STK31-induced proliferation and cell cycle progression in lung cancer cells. Inhibiting c-myc and TRRAP significantly decreased the expression of STK31, and a chromatin immunoprecipitation (ChIP) assay confirmed that c-myc directly bound to the STK31 promoter. These results indicated that STK31 may act as an oncogene in lung cancer and that c-myc may be the transcription factor that promotes STK31 expression. Moreover, the results suggested that c-myc can also regulate STK31 expression in a positive feedback loop, and the downregulation of STK31 in lung cancer cells had an inhibitory effect on cell viability, cell proliferation and cell cycle progression, likely by inactivating the Wnt/β-catenin pathway and positive feedback regulation by c-myc.

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“…FBLN1 is a member of family of extracellular glycoproteins that regulates cell morphology, cell migration, and cell interaction with extracellular matrix [30,31]. The tumorsuppressing role of FBLN1 has been described in many types of cancers like gastric carcinoma, prostate cancer, breast cancers, and ovarian cancers [32].…”

Section: Discussionmentioning

confidence: 99%

Upregulated Fibulin-1 Increased Endometrial Stromal Cell Viability and Migration by Repressing EFEMP1-Dependent Ferroptosis in Endometriosis

Yue

Song

Chen

et al. 2022

BioMed Research International

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Endometriosis (EMS) is a prevalent disease in women characterized by the presence of endometrial stroma and glands outside the uterus. Recent studies have showed that EMS is correlated with the resistance of endometrial stromal cells (ESCs) to ferroptosis, an iron-dependent nonapoptotic cell death. Fibulin-1 (FBLN1) is a newly identified target regulated by progesterone in the process of ESC decidualization. However, the role of FBLN1 in regulating ESC ferroptosis and EMS remains unclear. In the present study, the gene expression profiles of GSE58178, GSE23339, and GSE25628 were downloaded from the Gene Expression Omnibus (GEO) database, and the commonly differential genes were identified using Venn diagram analysis. The role of FBLN1 in ESC viability and migration was evaluated using Cell Counting Kit-8, transwell, and western blot analysis. We found that the FBLN1 expression was increased significantly in eutopic and ectopic endometrial tissues of patients with EMS compared with normal endometrium. FBLN1 overexpression in normal ESCs (NESCs) promoted cell viability and migration, whereas FBLN1 inhibition in ectopic ESCs (EESCs) decreased cell viability and migration. Furthermore, FBLN1 inhibition facilitated EESC death by triggering ferroptosis, as evidenced by increased Fe2+, lipid ROS, and malondialdehyde (MDA) level and decreased glutathione peroxidase 4 (GPX4) expression and glutathione (GSH) level. Mechanistically, FBLN1 interacted with EGF-containing fibulin-like extracellular matrix protein 1 (EFEMP1) and increased the protein stability of EFEMP1. More importantly, EFEMP1 silencing repressed the effect of FBLN1 on regulating EESC ferroptosis, death, and migration. Taken together, these results verify the role of the FBLN1/EFEMP1/ferroptosis pathway in the pathogenesis of EMS, and silencing of FBLN1/EFEMP1 might be an effective approach to treat EMS.

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Serum FBLN1 and STK31 as biomarkers of colorectal cancer and their ability to noninvasively differentiate colorectal cancer from benign polyps

Cited by 18 publications

References 18 publications

Construction of 2DE-Patterns of Plasma Proteins: Aspect of Potential Tumor Markers

Construction of 2DE-Patterns of Plasma Proteins: Aspect of Potential Tumor Markers

STK31 regulates the proliferation and cell cycle of lung cancer cells via the Wnt/β‑catenin pathway and feedback regulation by c‑myc

Upregulated Fibulin-1 Increased Endometrial Stromal Cell Viability and Migration by Repressing EFEMP1-Dependent Ferroptosis in Endometriosis

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