Malignant tumors pose a serious threat to human health and have high fatality rates. Conventional clinical anti-tumor treatment is mainly based on traditional surgery, chemotherapy, radiotherapy, and interventional therapy, and even though these treatment methods are constantly updated, a satisfactory efficacy is yet to be obtained. Therefore, research on novel cancer treatments is being actively pursued. We review the classification of gene therapies of malignant tumors and their advantages, as well as the development of gene editing techniques. We further reveal the nano-drug delivery carrier effect in improving the efficiency of gene editing. Finally, we summarize the progress in recent years of gene editing techniques based on nano-drug delivery carriers in the treatment of various malignant tumors, and analyze the prospects of the technique and its restricting factors.

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C26H26CdN4O4, monoclinic, P21/c (no. 14), a = 12.1676(8) Å, b = 13.4592(9) Å, c = 15.5782(10) Å, β = 112.1310(10) Å, V = 2363.2(3) Å3, Z = 4, Rgt(F) = 0.0244, wRref(F2) = 0.0584, T = 293(2) K.

BACKGROUND: Gastric cancer (GC) is the most common malignancy of the digestive system, causing over two hundred thousand deaths annually in China and over 750,000 deaths worldwide. The high invasiveness and metastatic rates are mainly responsible for mortality due to GC. Thus, it is an urgent priority to explore the mechanisms underlying GC metastasis to improve cancer diagnosis develop more effective biological targeting agents. METHODS: High-throughput RNA sequencing, quantitative PCR (q-PCR) and immunohistochemistry were used to compare PGAM1 levels in lymph node metastasis (LNM) tissues and carcinoma in situ (CIS) and noncancerous tissues from GC patients and correlated PGAM1 expression with patient prognosis, disease recurrence and mortality. In two GC cell lines (SGC7901 and BGC823) with sh-RNA-mediated PGAM1 knockdown, we analyzed cell growth in vitro, apoptosis and cell cycle progression by flow cytometry, and cell migration in wound-healing studies and transwell assays. In vivo subcutaneous growth of control and PGAM1 knockdown GC cell lines was measured in immunodeficient mice, and the potential role of PGAM1 in the expression of metastatic proteins and activation of migratory signaling was determined by flow cytometry and phospho-western blot analysis. RESULTS: We found that elevated PGAM1 expression in LNM, but not CIS tissues correlated with increased disease recurrence and death of GC patients. PGAM1 knockdown impaired proliferation, cell cycle progression and migration of GC cell lines. In a murine xenograft model, GC cells with a PGAM1 knockdown displayed decreased growth capacity in vivo relative to control cells. Western blot and flow cytometry analysis showed that PGAM1 knockdown in SGC7901 and BGC823 decreased the expression of metalloproteinases MMP2 and MMP9 as well as the adhesion molecule ICAM-I, and impaired phosphorylation of Src, FAK and Paxillin relative to parental cells. CONCLUSIONS: Our results indicate that PGAM1 is a novel biomarker of metastatic GC and may play an important role in promoting GC lymph node metastasis by driving cell proliferation, activating cytoskeletal reorganization and cell migration through the Src/FAK/Paxillin pathway and promoting digestion of the extracellular matrix by upregulating the expression of MMP2 and MMP9.