Knockdown of ferritin heavy chain (FTH) inhibits the migration of prostate cancer through reducing S100A4, S100A2, and S100P expression

Lu, Cuixiu; Zhao, Huijun; Luo, Chenshuo; Lei, Ting; Zhang, Man

doi:10.21037/tcr-19-2852

Cited by 7 publications

(7 citation statements)

References 41 publications

(63 reference statements)

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“…According to the analysis results of iTRAQ mass spectrometry technology, compared with the NC group cells, the top twelfth expression differences among down-regulated genes in FTH knockout PC3 cells are S100A4, CRABP1, S100A2, S100P, GDF15, FAM84B, KRT75, LYRM7, OCLN, LCP1, NDUFAB1, F2RL1. Among them, the connection between S100 family members and FTH and their possible effects on PC3 cells have been discussed in our previous studies [11]. In this study, the remaining other proteins will be further discussed and veri ed.…”

Section: Introductionmentioning

confidence: 75%

“…The previous research of our laboratory performed iTRAQ mass spectrometry analysis on FTH knockout PC3 cells (LV-shFTH PC3) and the negative control group [11]. The results of mass spectrometry analysis showed that a variety of proteins were differentially expressed.…”

Section: Results Of Differentially Expressed Proteins In Fth Knockout Pc3 Cells (Lv-shfth Pc3)mentioning

confidence: 99%

“…For example, epithelial mesenchymal transition (EMT) is a classic process involving members of the S100 family. The molecular mechanism of these three proteins in FTH-induced changes in the migration ability of PCa cells has been discussed in our previous studies [11], so we will not discuss them here.…”

Section: Proteins Related To Tumor Cell Migration and Invasionmentioning

confidence: 99%

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Mechanism of Ferritin Heavy Chain in the Proliferation and Migration of Prostate Cancer Cells

Zhao

Zhang

2021

Preprint

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Ferritin is an important molecule in the regulation of cell proliferation, growth inhibition escape, cell death inhibition and angiogenesis. More and more studies have given evidence of abnormal iron metabolism in tumors. Whether ferritin can be a new type of marker for early diagnosis of tumorous diseases remains to be explored. In this study, we verified the expression level of ferritin heavy chain (FTH) in benign prostatic hyperplasia epithelial cell (BPH-1) and three kinds of PCa cells by Western blotting. Lentivirus was used to construct FTH gene overexpression vector, then construct FTH overexpression PCa cell lines. Meanwhile, LNCaP cells and DU145 cells FTH silent expression prostate cancer cell lines were constructed using Crispr Cas9 technology. Next, clone proliferation experiments, transwell experiments, and scratch experiments were used to verify the cell proliferation, invasion, and migration capabilities of each group of cells with different FTH expression levels. The FTH knockout PC-3 cell (LV-shFTH PC3) has been established in our laboratory. Make full use of the existing results from Isobaric Tag for Relative and Absolute Quantitation (iTRAQ) mass spectrometry technology to analyze differentially expressed protein analysis between LV-shFTH PC3 cells and control cells. Combine GO analysis to select the target protein for subsequent cell protein expression level verification. Our results show that FTH overexpression can promote the proliferation, migration and invasion of prostate cancer cell lines, while FTH knockout causes the opposite result. Combined with mass spectrometry (MS) detection, it is speculated that FTH may trigger changes in cell behavior by regulating the expression of the following proteins: S100A4, CRABP1, S100A2, S100P, GDF15, FAM84B, KRT75, LYRM7, OCLN, LCP1, F2RL1. (The study is not a clinical trial, no registration number and registration date are required)

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Section: Introductionmentioning

confidence: 75%

Section: Results Of Differentially Expressed Proteins In Fth Knockout Pc3 Cells (Lv-shfth Pc3)mentioning

confidence: 99%

Section: Proteins Related To Tumor Cell Migration and Invasionmentioning

confidence: 99%

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Mechanism of Ferritin Heavy Chain in the Proliferation and Migration of Prostate Cancer Cells

Zhao

Zhang

2021

Preprint

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“…Ferritin modulates the proliferation, apoptosis and invasion of cancer cells [72]. Therefore, its levels are dysregulated in many human tumors, such as breast cancer [73], prostate cancer [74] and glioblastoma [75], and are associated with poor survival rates in multiple cancers [72]. The enhanced expression of FTH1 in HCCLM3 and MHCC97H hepatocarcinoma cells leads to increased cell proliferation via the downregulation of H 2 O 2 and ROS levels [76].…”

Section: Ferritinmentioning

confidence: 99%

Iron Metabolism in Cancer and Senescence: A Cellular Perspective

Crescenzi

Leonardi

Pacifico

2023

Biology

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Iron participates in a number of biological processes and plays a crucial role in cellular homeostasis. Alterations in iron metabolism are considered hallmarks of cancer and drivers of aggressive behaviors, such as uncontrolled proliferation, resistance to apoptosis, enhanced metastatic ability, increased cell plasticity and stemness. Furthermore, a dysregulated iron metabolism has been associated with the development of an adverse tumor microenvironment. Alterations in iron metabolism have been described in cellular senescence and in aging. For instance, iron has been shown to accumulate in aged tissues and in age-related diseases. Furthermore, in vitro studies demonstrate increases in iron content in both replicative and stress-induced senescent cells. However, the role, the mechanisms of regulation and dysregulation and the effects of iron metabolism on senescence remain significantly less characterized. In this review, we first provide an overview of iron metabolism and iron regulatory proteins. Then, we summarize alterations in iron homeostasis in cancer and senescence from a cellular point of view.

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“…A delicate balance must be maintained by the malignant cells in order to maintain an appropriately dysregulated iron metabolism, as too much or too little iron can have adverse effects on cell viability. FTH1 expression is a key iron-regulatory gene that impacts cytosolic LIP, which if significantly perturbed may affect cancer growth [48][49][50]. Indeed, access to bioavailable iron can be directly altered through modulating the expression of both FTH1 and TFRC.…”

Section: Introductionmentioning

confidence: 99%

Assessing the Potential of Small Peptides for Altering Expression Levels of the Iron-Regulatory Genes FTH1 and TFRC and Enhancing Androgen Receptor Inhibitor Activity in In Vitro Prostate Cancer Models

Currie,

Bjerknes,

Myklebust

et al. 2023

IJMS

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Recent research highlights the key role of iron dyshomeostasis in the pathogenesis of prostate cancer (PCa). PCa cells are heavily dependent on bioavailable iron, which frequently results in the reprogramming of iron uptake and storage pathways. Although advanced-stage PCa is currently incurable, bioactive peptides capable of modulating key iron-regulatory genes may constitute a means of exploiting a metabolic adaptation necessary for tumor growth. Recent annual increases in PCa incidence have been reported, highlighting the urgent need for novel treatments. We examined the ability of LNCaP, PC3, VCaP, and VCaP-EnzR cells to form colonies in the presence of androgen receptor inhibitors (ARI) and a series of iron-gene modulating oligopeptides (FT-001-FT-008). The viability of colonies following treatment was determined with clonogenic assays, and the expression levels of FTH1 (ferritin heavy chain 1) and TFRC (transferrin receptor) were determined with quantitative polymerase chain reaction (PCR). Peptides and ARIs combined significantly reduced PCa cell growth across all phenotypes, of which two peptides were the most effective. Colony growth suppression generally correlated with the magnitude of concurrent increases in FTH1 and decreases in TFRC expression for all cells. The results of this study provide preliminary insight into a novel approach at targeting iron dysmetabolism and sensitizing PCa cells to established cancer treatments.

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Knockdown of ferritin heavy chain (FTH) inhibits the migration of prostate cancer through reducing S100A4, S100A2, and S100P expression

Cited by 7 publications

References 41 publications

Mechanism of Ferritin Heavy Chain in the Proliferation and Migration of Prostate Cancer Cells

Mechanism of Ferritin Heavy Chain in the Proliferation and Migration of Prostate Cancer Cells

Iron Metabolism in Cancer and Senescence: A Cellular Perspective

Assessing the Potential of Small Peptides for Altering Expression Levels of the Iron-Regulatory Genes FTH1 and TFRC and Enhancing Androgen Receptor Inhibitor Activity in In Vitro Prostate Cancer Models

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