Reduced Lipocalin 2 Expression Contributes to Vincristine Resistance in Human Colon Cancer Cells

Guo, Xiaotong; Qin, Li; Wang, Yanfang; Wang, Tianyun; Chen, Si-Jia; Tian, Zheng-Wei

doi:10.2174/1574892813666171221120504

Cited by 4 publications

(2 citation statements)

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“…And knocking out lipocalin2 in HCT-8 CRC cell induces tumor cell resistant to vincristine. These findings imply that lipocalin2 plays different roles in different cell lines and these effects can not be applied universally (87). Because lipocalin2 regulates iron metabolism bilaterally, tumor cells can use it to uptake more iron to meet their metabolic needs while also excreting iron from the cytoplasm in the form of the Fe-lipocalin2 complex.…”

Section: Lipocalin2mentioning

confidence: 99%

Iron metabolism in colorectal cancer

Huang

et al. 2023

Front. Oncol.

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Iron, as one of the essential trace elements in the human body, is involved in a wide range of critical biochemical reactions and physiological processes, including the maintenance of the normal cell cycle, mitochondrial function, nucleotide metabolism, and immune response. In this context, iron is naturally associated with cancer occurrence. Cellular iron deficiency can induce apoptosis, however, iron can also engage in potentially harmful reactions that produce free radicals because of its capacity to gain and lose electrons. Studies suggest that dietary iron, particularly heme iron, may be one of the leading causes of colorectal cancer (CRC). Moreover, patients with CRC have abnormal iron absorption, storage, utilization, and exportation. Therefore, iron is crucial for the development and progression of CRC. Elaborating on the alterations in iron metabolism during the onset and advancement of CRC would help to further explain the role and mechanism of iron inside the body. Thus, we reviewed the alterations in numerous iron metabolism-related molecules and their roles in CRC, which may provide new clues between iron metabolism and CRC.

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Section: Lipocalin2mentioning

confidence: 99%

Iron metabolism in colorectal cancer

Huang

et al. 2023

Front. Oncol.

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“…Many anti-cancer natural compounds derived from plant sources, such as resveratrol, camptothecin, capsaicin, and catechin, have been extensively studied [10,11]. Moreover, paclitaxel and vincristine have been clinically applied as rstline drugs in cancer therapy [12,13]. Corosolic acid (CA) is a pentacyclic triterpenoid that is found in kiwi, crape myrtle, loquat, and other plants.…”

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confidence: 99%

Transcriptome and Proteome Analysis Reveals Corosolic Acid Inhibiting Bladder Cancer via Targeting Cell Cycle and Inducing Mitophagy in Vitro and in Vivo

Cui

et al. 2021

Preprint

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Background Existing chemotherapy and radiotherapy methods have drawbacks such as high toxicity, high side effects, poor efficacy, and chemoresistance. Therefore, there is an urgent need to develop new anti-cancer drugs with low toxicity and high efficiency for cancer therapy and the prevention of recurrence. Corosolic acid (CA) is a medicine and food homologue and has many biological activities of health care. However, the anti-tumor effects and mechanism of CA in bladder cancer remain unexplored. Methods To study the anticancer effect of CA on bladder cancer cells, CCK8, EdU, high-content living cell imaging experiments were performed. And the mice model was used to verify the anticancer effect and toxicity for mice. To investigate the molecular mechanism of CA inhibition on bladder cancer cells, transcriptomics and proteomics were employed. To further verify the pharmacological mechanism, flow cytometry, RT-qPCR, western blotting and immunofluorescence staining experiments were performed, and the CA targeting molecules were analyzed in combination with our experimental and public clinical data. Results We found that CA inhibited bladder cancer cell proliferation in a concentration- and time-dependent manner. Xenograft experiments showed that CA inhibited the growth of subcutaneous tumors, and had no toxicity in mice. Integration of omics analysis revealed that low concentrations of CA inhibited bladder cancer cells proliferation via attenuating DNA synthesis by downregulating TOP2A and LIG1, and via diminishing mitosis by downregulating CCNA2, CCNB1, CDC20, and RRM2. High concentrations of CA induced cell death not through the apoptotic pathway but through triggering mitophagy pathway via upregulating SQSTM1/P62, NBR1, and UBB. Conclusions CA, a natural compound homologous to medicine and food, inhibits the mitosis of bladder cancer cells at low concentrations, and kills bladder cancer cells by inducing mitophagy at high concentrations. This study provides a comprehensive understanding of the pharmacological mechanism of CA inhibition in bladder cancer for the first time, which is helpful for the development of new anti-tumor drugs based on CA.

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TUFT1 Facilitates Metastasis, Stemness, and Vincristine Resistance in Colorectal Cancer via Activation of PI3K/AKT Pathway

Yang

Zhang

2021

Biochem Genet

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Reduced Lipocalin 2 Expression Contributes to Vincristine Resistance in Human Colon Cancer Cells

Abstract: Overall, these results demonstrate that LCN2 plays an important role in VCR resistance and is a potential therapeutic target for this disease.

Cited by 4 publications

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Iron metabolism in colorectal cancer

Iron metabolism in colorectal cancer

Transcriptome and Proteome Analysis Reveals Corosolic Acid Inhibiting Bladder Cancer via Targeting Cell Cycle and Inducing Mitophagy in Vitro and in Vivo

TUFT1 Facilitates Metastasis, Stemness, and Vincristine Resistance in Colorectal Cancer via Activation of PI3K/AKT Pathway

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