Polyolefins,
the largest used commodity plastics in the world,
find extensive application in many fields. However, most end up in
landfills or incineration, leading to severe ecological crises, environmental
pollution, and serious resource waste problems. As representatives
on chemical upcycling of polyolefin plastics polyolefin waste to fuels
and bulk/fine chemicals, polyolefin catalytic cracking and hydrocracking
based on zeolite or metal/zeolite composite catalysts are considered
the most effective paths due to their large capacity and strong adaptability
to existing petrochemical equipment. After an overview of the reaction
mechanisms of pyrolysis and catalytic cracking, this review aims to
comprehensively discuss the influence of zeolite catalyst structure
(acidity, pore structure, and morphology) on the catalytic activity,
selectivity, and stability of polyolefin cracking, particularly emphasizing
the importance for matching acidity and pore structure for target
product formation. Subsequently, the structure–activity relationship
between the metal site and zeolite’s acid site in polyolefin
hydrocracking is also discussed. In the end, emerging opportunities
and challenges are proposed to promote a more efficient way for polyolefin
chemical upcycling.
Colon cancer is the third most common cancer worldwide. Many miRNAs have been reported to be involved in colon cancer progression. However, there are only a few studies on the role of miR-219a-1 in colon cancer, and the molecular mechanisms involved remain unclear. The aim of this study was to investigate the miR-219a-1 level in patients with colon cancer and to explore both the effects and regulatory mechanisms of miR-219a-1 in the malignancy of colon cancer cells. Real-time PCR and western blot analysis were used to analyze the expression levels of miR-219a-1 and mediator of ErbB2-driven cell motility 1. Cell Counting Kit-8, transwell and wound-healing assays were performed to investigate the malignant ability of colon cancer cells. A luciferase assay was performed to explore whether miR-219a-1 could directly bind to 3ʹ-UTR region of MEMO1. miR-219a-1 was found to be downregulated in colon cancer cell lines and in patients with colon cancer. Additionally, miR-219a-1 could inhibit colon cancer cell proliferation, invasion and migration. We identified MEMO1 as a novel potential target gene of miR-219a-1. Luciferase assays showed that miR-219a-1 could directly bind to 3′-UTR of MEMO1. Overexpression of miR-219a-1 in colon cancer cells could inhibit the expression of MEMO1. Furthermore, MEMO1 was upregulated in patients with colon cancer, which was inversely correlated with miR-219a-1 levels. In conclusion, our study revealed that miR-219a-1 exerts anti-tumor effects and regulates colon cancer cell proliferation, invasion and migration by targeting MEMO1, suggesting that miR-219a-1 could act as a therapeutic target in colon cancer.
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