Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 20 de 59
Filter
1.
Acta Pharmaceutica Sinica B ; (6): 1315-1328, 2021.
Article in English | WPRIM | ID: wpr-881201

ABSTRACT

Bcr-Abl threonine 315 to isoleucine 315 (T315I) gatekeeper mutation induced drug resistance remains an unmet clinical challenge for the treatment of chronic myeloid leukemia (CML). Chemical degradation of Bcr-Abl

2.
Acta Pharmaceutica Sinica B ; (6): 488-504, 2021.
Article in English | WPRIM | ID: wpr-881149

ABSTRACT

Medulloblastoma (MB) is a common yet highly heterogeneous childhood malignant brain tumor, however, clinically effective molecular targeted therapy is lacking. Modulation of hedgehog (HH) signaling by epigenetically targeting the transcriptional factors GLI through bromodomain-containing protein 4 (BRD4) has recently spurred new interest as potential treatment of HH-driven MB. Through screening of current clinical BRD4 inhibitors for their inhibitory potency against glioma-associated oncogene homolog (GLI) protein, the BRD4 inhibitor

3.
Acta Pharmaceutica Sinica B ; (6): 156-180, 2021.
Article in English | WPRIM | ID: wpr-881131

ABSTRACT

@#This study was aimed to design the first dual-target small-molecule inhibitor co-targeting poly (ADP-ribose) polymerase-1 (PARP1) and bromodomain containing protein 4 (BRD4), which had important cross relation in the global network of breast cancer, reflecting the synthetic lethal effect. A series of new BRD4 and PARP1 dual-target inhibitors were discovered and synthesized by fragment-based combinatorial screening and activity assays that together led to the chemical optimization. Among these compounds, 19d was selected and exhibited micromole enzymatic potencies against BRD4 and PARP1, respectively. Compound 19d was further shown to efficiently modulate the expression of BRD4 and PARP1. Subsequently, compound 19d was found to induce breast cancer cell apoptosis and stimulate cell cycle arrest at G1 phase. Following pharmacokinetic studies, compound 19d showed its antitumor activity in breast cancer susceptibility gene 1/2 (BRCA1/2) wild-type MDA-MB-468 and MCF-7 xenograft models without apparent toxicity and loss of body weight. These results together demonstrated that a highly potent dual-targeted inhibitor was successfully synthesized and indicated that co-targeting of BRD4 and PARP1 based on the concept of synthetic lethality would be a promising therapeutic strategy for breast cancer.

4.
Article in English | WPRIM | ID: wpr-878339

ABSTRACT

Objective@#Cervical cancer (CC) is one of the most common malignant tumors in gynecology. This study aimed to investigate the prognostic significance of serum microRNA (miR)-378a-3p in CC and the effect of miR-378a-3p on tumor growth.@*Methods@#Real-time quantitative polymerase chain reaction analysis was used to measure the expression of miR-378a-3p in serum from patients with CC and healthy control subjects as well as from CC tissues and adjacent normal tissues. The association between serum miR-378a-3p levels and clinicopathological factors was analyzed. The correlation between miR-378a-3p levels and overall survival (OS) of CC patients was determined by Kaplan-Meier analysis. The CC cell proliferation and migration abilities after transfection of miR-378a-3p mimics were detected by Cell Counting Kit-8 and scratch wound healing assays, respectively. Tumor volume and weight in mice treated with miR-378a-3p were measured using a caliper and an electronic balance.@*Results@#MiR-378a-3p expression was downregulated in the serum and tissues of CC patients compared to that in healthy control subjects and normal tissues, respectively. Low expression of miR-378a-3p was positively correlated with large tumor size, advanced tumor stage, and lymph node metastasis. The OS of patients with low expression of miR-378a-3p was significantly lower than that of patients with high expression. Overexpression of miR-378a-3p suppressed the proliferation and migration of CC cells. @*Conclusion@#MiR-378a-3p downregulation is associated with the development and prognosis of CC, suggesting that it may be a potential biomarker for CC.


Subject(s)
Animals , Biomarkers/blood , Cell Movement , Cell Proliferation , Down-Regulation , Female , Gene Expression Regulation, Neoplastic , Humans , Mice , Mice, Inbred BALB C , MicroRNAs/blood , Middle Aged , Uterine Cervical Neoplasms/metabolism
5.
Acta Pharmaceutica Sinica ; (12): 2785-2792, 2020.
Article in Chinese | WPRIM | ID: wpr-862277

ABSTRACT

Reactive nitrogen species (RNS) affects intracellular redox balance and induces post-translational modification of proteins. Moreover, RNS, as the signal molecule, participates in the transduction of cellular signals under physiological conditions. However, excessive RNS can induce nitrosative stress and then damage cells, and thereby may play a role in the tumor initiation and progression. Thus, we discussed the role of RNS under physiological conditions and the tumor microenvironment, which may provide some novel ideas for the development of new drugs and the treatment of diseases.

6.
Chinese Pharmaceutical Journal ; (24): 979-984, 2020.
Article in Chinese | WPRIM | ID: wpr-857665

ABSTRACT

Chemotherapeutic drugs play an important role in the treatment of cancer, but the individual differences of patients' sensitivity to chemotherapeutic drugs and the drug resistance of chemotherapeutic drugs have always been a thorny problem in clinical treatment. Recent studies have shown that gut microbiota plays a key role in regulating the efficacy of chemotherapeutic drugs. Gut microbiota can regulate host response to chemotherapy through a variety of mechanisms, including immune interaction, heterogeneous metabolism and changes in community structure. This paper introduces the effects of traditional chemotherapeutic drugs and new immunotherapeutic drugs, such as anti-CTLA-4 and anti-PD-1 antibodies, on gut microbiota, as well as their effects on chemotherapeutic efficacy and mechanism, in order to provide evidences and clues for cancer treatments targeting gut microbiota.

7.
Article in Chinese | WPRIM | ID: wpr-843094

ABSTRACT

Objective: To investigate the effect of toosendanin (TSN) on the growth and invasion of gastric cancer cells BGC-823 by regulating circDLST expression. Methods: After gastric cancer cells BGC-823 were exposed to different con-centrations of TSN (0, 0.5, 1.0, and 2.0 μmol/L) for 24 h, quantitative PCR was used to detect the expression of circDLST. BGC-823 cells were transfected with the circDLST overexpression lentiviral vector or its control vector (CON), and then treated with 0.5 μmol/L TSN or PBS. So the cells were divided into circDLST+TSN group, CON+TSN group and CON+PBS group. The viability and invasive potential of BGC-823 cells were observed by MTT proliferation test and Transwell invasion assay. The subcutaneous transplanted tumor models were established by using circDLST-transfected cell line BGC-823 or the control cell line in nude mice, and then 200 μg/kg TSN or the same volume of PBS was injected intraperitoneally every day. So the mice were divided into circDLST+TSN group, CON+TSN group and CON+PBS group. Results: Compared with the control group (0 μmol/L), all 3 concentrations of TSN decreased the expression levels of circDLST in a concentration dependent manner (P<0.01). TSN could significantly reduce the cell viability, cell invasion and subcutaneous xenograft tumor growth (P=0.000), while circDLST overexpression reversed the inhibitory effect of TSN (P<0.01). Conclusion: TSN may inhibit the growth and invasion of gastric cancer cells BGC-823 by downregulating circDLST expression.

8.
Acta Pharmaceutica Sinica B ; (6): 1294-1308, 2020.
Article in English | WPRIM | ID: wpr-828807

ABSTRACT

A great challenge in multi-targeting drug discovery is to identify drug-like lead compounds with therapeutic advantages over single target inhibitors and drug combinations. Inspired by our previous efforts in designing antitumor evodiamine derivatives, herein selective histone deacetylase 1 (HDAC1) and topoisomerase 2 (TOP2) dual inhibitors were successfully identified, which showed potent and antitumor potency. Particularly, compound was orally active and possessed excellent antitumor activity in the HCT116 xenograft model (TGI = 75.2%, 150 mg/kg, .) without significant toxicity, which was more potent than HDAC inhibitor vorinostat, TOP inhibitor evodiamine and their combination. Taken together, this study highlights the therapeutic advantages of evodiamine-based HDAC1/TOP2 dual inhibitors and provides valuable leads for the development of novel multi-targeting antitumor agents.

9.
Acta Pharmaceutica Sinica B ; (6): 1453-1475, 2020.
Article in English | WPRIM | ID: wpr-828796

ABSTRACT

Angiokinases, such as vascular endothelial-, fibroblast- and platelet-derived growth factor receptors (VEGFRs, FGFRs and PDGFRs) play crucial roles in tumor angiogenesis. Anti-angiogenesis therapy using multi-angiokinase inhibitor has achieved great success in recent years. In this study, we presented the design, synthesis, target identification, molecular mechanism, pharmacodynamics (PD) and pharmacokinetics (PK) research of a novel triple-angiokinase inhibitor WXFL-152. WXFL-152, identified from a series of 4-oxyquinoline derivatives based on a structure-activity relationship study, inhibited the proliferation of vascular endothelial cells (ECs) and pericytes by blocking the angiokinase signals VEGF/VEGFR2, FGF/FGFRs and PDGF/PDGFR simultaneously . Significant anticancer effects of WXFL-152 were confirmed in multiple preclinical tumor xenograft models, including a patient-derived tumor xenograft (PDX) model. Pharmacokinetic studies of WXFL-152 demonstrated high favourable bioavailability with single-dose and continuous multi-dose by oral administration in rats and beagles. In conclusion, WXFL-152, which is currently in phase Ib clinical trials, is a novel and effective triple-angiokinase inhibitor with clear PD and PK in tumor therapy.

10.
Acta Pharmaceutica Sinica B ; (6): 529-545, 2020.
Article in English | WPRIM | ID: wpr-792991

ABSTRACT

The limited penetration of nanoparticles and their poor accessibility to cancer cell fractions in tumor remain essential challenges for effective anticancer therapy. Herein, we designed a targeting peptide-decorated biomimetic lipoprotein (termed as BL-RD) to enable their deep penetration and efficient accessibility to cancer cell fractions in a tumor, thereby improving the combinational chemo-photodynamic therapy of triple negative breast cancer. BL-RD was composed of phospholipids, apolipoprotein A1 mimetic peptide (PK22), targeting peptide-conjugated cytotoxic mertansine (RM) and photodynamic agents of DiIC18(5) (DiD). The counterpart biomimetic lipoprotein system without RM (termed as BL-D) was fabricated as control. Both BL-D and BL-RD were nanometer-sized particles with a mean diameter of less than 30 nm and could be efficiently internalized by cancer cells. After intravenous injection, they can be specifically accumulated at tumor sites. When comparing to the counterpart BL-D, BL-RD displayed superior capability to permeate across the tumor mass, extravasate from tumor vasculature to distant regions and efficiently access the cancer cell fractions in a solid tumor, thus producing noticeable depression of the tumor growth. Taken together, BL-RD can be a promising delivery nanoplatform with prominent tumor-penetrating and cancer cells-accessing capability for effective tumor therapy.

11.
Article in Chinese | WPRIM | ID: wpr-817801

ABSTRACT

Objective To investigate the effect of medical sodium hyaluronate gel (HA) on the growth and metastasis of abdominal and pelvic tumor cells in vitro and in nude mice. Methods Three tumor cells, Hela, CT26 and HCT116, were used to investigate the effects of different HA concentrations on the growth and migration of tumor cells in vitro by MTT assay and Transwell assay. An orthotopic transplantation model of colonic tumor in nude mice was established to investigate the effect on the proliferation of cell HCT116 by comparing the tumor volume and tumor mass 4 weeks after inoculation. The effects on the metastasis of cell CT26 were investigated by comparing the tumor metastasis rate and the number of metastatic lesions of lung and liver in nude mice among the different experimental groups 3 weeks after inoculation. Results HA did not promote the growth and metastasis of Hela, CT26 and HCT116 cells in vitro at different concentrations. Actually, HA exhibited a certain inhibitory activity at the concentration of 5 mg/ml. In the orthotopic transplantation model of colonic tumor-HCT116, HA did not promote the growth of cell HCT116. In the orthotopic transplantation model of colonic tumor-CT26, HA inhibited CT26 tumor metastasis. Conclusion Under the experimental conditions, HA did not promote the growth, migration or metastasis of abdominal and pelvic related tumor cells including Hela, CT26 and HCT116 in vitro and in vivo.

12.
Journal of Medical Biomechanics ; (6): E145-E152, 2019.
Article in Chinese | WPRIM | ID: wpr-802485

ABSTRACT

Objective To study the effect of intercellular adhesion of tumor cells on immune response of human body. Methods A tumor growth-cellular immune feedback model was developed based on cellular Potts model (CPM) to simulate the progression of tumor cells and the cellular immune feedback system, and the influence of adhesion between tumor cells on the immune system was analyzed. Results Under the condition of tumor intercellular adhesion with normal intensity, tumor cells could escape when the immune system was weak and be eliminated when the immune system was strong. Under the condition of tumor intercellular adhesion with low intensity, tumor cells could escape when the immune system was weak, while exhibited behavior of oscillation and could not be eliminated when the immune system was strong. Conclusions Higher adhesion between tumor cells inhibited escape of tumor cells from the immune system, while lower adhesion between tumor cells could effectively help the tumor escape killing from the immune system. When the tumor was extremely spread, the immune system could not completely eliminate tumor cells.

13.
Electron. j. biotechnol ; 32: 13-18, Mar. 2018. ilus, graf
Article in English | LILACS | ID: biblio-1022495

ABSTRACT

Background: The suppression of cancer cell growth and invasion has become a challenging clinical issue. In this study, we used nanotechnology to create a new drug delivery system to enhance the efficacy of existing drugs. We developed layered double hydroxide by combing Au nanosol (LDH@Au) and characterized the compound to prove its function as a drug delivery agent. The anti-cancer drug Doxorubicin was loaded into the new drug carrier to assess its quality. We used a combination of apoptosis assays, cell cycle assays, tissue distribution studies, cell endocytosis, transwell invasion assays, and immunoblotting to evaluate the characteristics of LDH@Au as a drug delivery system. Results: Our results show that the LDH@Au-Dox treatment significantly increased cancer cell apoptosis and inhibited cell invasion compared to the control Dox group. Additionally, our data indicate that LDH@Au-Dox has a better target efficiency at the tumor site and improved the following: cellular uptake, anti-angiogenesis action, changes in the cell cycle, and increased caspase pathway activation. Conclusions: Our findings suggest the nano drug is a promising anti-cancer agent and has potential clinical applications.


Subject(s)
Stomach Neoplasms/drug therapy , Doxorubicin/administration & dosage , Apoptosis/drug effects , Nanoparticles/administration & dosage , Antibiotics, Antineoplastic/administration & dosage , Doxorubicin/pharmacology , Cell Cycle/drug effects , Blotting, Western , Drug Delivery Systems , Nanotechnology , Cell Line, Tumor , Microscopy, Electron, Transmission , Cell Proliferation/drug effects , Endocytosis/drug effects , Hydroxides , Antibiotics, Antineoplastic/pharmacology , Neoplasm Invasiveness/prevention & control
14.
Chinese Journal of Immunology ; (12): 558-563, 2018.
Article in Chinese | WPRIM | ID: wpr-702774

ABSTRACT

Objective: To evaluate the effects of ropivacaine on cell proliferation and tumor growth of colon carcinoma. Methods: CCK8 assay was performed for cell viability. The colony formation assay was performed for cell proliferation. Cell flow apoptosis and cell cycle were measured by Flow cytometry. Protein levels were calculated by Western blot. Meanwhile,nude mice were inoculated with SW480 colon cells and treated with ropivacaine. Tumor volume and survival rate were examined after treatment. Results: The results of CCK8 showed that the optimum concentrations of ropivacaine were 20, 50 and 100 μg/ ml respectively. Ropivacaine dose-dependently inhibited colony formation (17. 80±0. 51,P<0. 001) and expressions of Ki67 (0. 32±0. 68, P<0. 01) and PCNA(0. 14±0. 24,P<0. 01). Meanwhile,treatment with ropivacaine markedly increased apoptosis (12. 80±1. 24,P< 0. 01) and protein levels of caspase-3(1. 76±1. 43,P <0. 001) and caspase-9 (1. 61±1. 26,P <0. 001) . In addition,ropivacaine notably induced cell cycle arrest (40. 5%,P<0. 01),expression of p53 (1. 16±0. 65,P<0. 01),and down-regulated the expression level of Cyclin A (0. 12±0. 12,P<0. 05) . Furthermore,ropivacaine inhibited tumor growth (1 247. 60±1. 37,P<0. 01),up-regulated survival rate of mice and induced apoptosis of tumor tissue (78. 00 ±1. 45,P <0. 001) in a dose-depended manner. Conclusion: Ropivacaine inhibits cell proliferation and tumor growth of colon cancer.

15.
Journal of Medical Postgraduates ; (12): 834-838, 2017.
Article in Chinese | WPRIM | ID: wpr-611717

ABSTRACT

Objective The role of long non-coding RNA Linc00467 in human lung adenocarcinoma is not yet clear.This study was to investigate the expression of long non-coding RNA Linc00467 in human lung adenocarcinoma, its clinical significance, and the effects of Linc00467 on the functions of the tumor and endothelial cells in vitro.Methods Lung adenocarcinoma tissue and normal tissue surrounding the malignance were obtained from 60 patients with pathologically proved stage I-Ⅲa lung adenocarcinoma.Human umbilical vein endothelial cells (HUVECs) were transfected with the over-expressed plasmid pccl-Linc00467 (HUVEC experimental group) or the empty vector pccl (HUVEC control group), A549 cells with Linc00467-siRNA (A549 experimental group) or negative siRNA (A549 control group), and H1299 cells, too, with Linc00467-siRNA (H1299 experimental group) or negative siRNA (H1299 control group).The expression level of Linc00467 in the lung adenocarcinoma tissue was detected by qRT-PCR with an analysis of its correlation with the clinicopathological characteristics of the patients;the influence of Linc00467 on the proliferation of the A549, H1299 and HUVEC cells was assayed with CCK-8;and the role of Linc00467 in the angiogenesis of the HUVECs was assessed by fibrin bead sprouting assay.Results The expression of Linc00467 in the lung adenocarcinoma tissue was 2.72±1.31 times as high as that in the normal lung tissue (P<0.01), and those in the A549 and H1299 cells were 3.45±0.25 and 3.22±0.33 times as high as those in the human bronchial epithelial (HBE) cells (P<0.01).The expression level of Linc00467 was significantly correlated with the tumor size and vascular invasion (P<0.05).After transfection of Linc00467-siRNA, the expressions of Linc00467 in the A549 and H1299 experimental groups were down-regulated by 72% and 68% as compared with those in the A549 and H1299 control groups (P<0.01).The number of living cells was remarkably decreased in the A549 experimental group in comparison with the A549 control at 48 h (1.29±0.07 vs 1.51±0.09), 72 h (1.53±0.15 vs 2.13±0.11), and 96 h after culturing (1.98±0.18 vs 3.02±0.12), and so was it in the H1299 experimental versus the H1299 control group, but markedly increased in the HUVEC experimental versus the HUVEC control group (P<0.05).At 5 days, HUVEC experimental group, as compared with the HUVEC control, showed a significantly increased number of newly formed vascular branches (7.36 vs 4.25/superbead, P<0.01) and relative length of the blood vessels (3.12 vs 1, P<0.01).Conclusion Linc00467 promotes tumor cell proliferation and angiogenesis and is highly expressed in the lung adenocarcinoma tissue, which is correlated with the tumor size and vascular invasion and suggests that Linc00467 could be a potential biomarker and therapeutic target.

16.
Article in Chinese | WPRIM | ID: wpr-610480

ABSTRACT

Objective · To establish human cervical cancer xenografts in nude mice and investigate the antitumor therapeutic effects and safety of EGF modified cisplatin-alginate conjugate liposomes. Methods · Cervical cancer-bearing mouse model was established by subcutaneously injecting Hela cells in nude mice. Generalstate and xenograft growth of the mice were observed. Tumor volumes, tumor weights, and the body weights of mice during the treatment were recorded and analyzed. The expression levels of EGFR in xenografts were detected by immunohistochemistry. Results · ① EGFR was highly expressed in the xenografts. ② CS-EGF-Lip inhibited the tumor growth effectively (P=0.000). ③ The inhibition rates of tumor volume and tumor weight of CS-EGF-Lip were 80.22% and 58.60% respectively, which were betterthan those of cisplatin (P=0.000). ④ CS-EGF-Lip had minimal influence on body weight in mice (P=0.000). Conclusion · CS-EGF-Lip has more effective antitumoreffects than cisplatin in cervical cancer-bearing mice, which can inhibit tumor growth of solid tumors with enhanced efficacy and safety.

17.
Article in Chinese | WPRIM | ID: wpr-658409

ABSTRACT

Cancer cell metabolic reprogramming is a highly significant feature in tumor development and progression.This process is an extension of aerobic glycolysis(i.e.,Warburg effect).The metabolic pattern,such as that of glycolysis,oxidative phosphorylation, amino acid metabolism,fatty acid metabolism,and nucleic acid metabolism,is altered significantly during cell carcinogenesis.Fatty ac-id metabolism is required for energy storage,membrane proliferation,and signaling molecule generation.Thus,studying the mecha-nism of de novo fatty acid synthesis and its relationship with the development and progression of tumor,as well as the use and target-ing of the key enzyme in this metabolic pathway,is vital for the diagnosis,prevention,and treatment of cancer.Herein,we provide a brief review of metabolic reprogramming in cancer cells.We focus on the pathways of de novo fatty acid synthesis during the develop-ment and progression of tumor.

18.
Article in Chinese | WPRIM | ID: wpr-658255

ABSTRACT

Objective To explore the influence of Mac-1 deficiency on tumor growth of melanoma. Methods The population of Mac-1 gene knock-out ( Mac-1 -/ -) mice was expanded. B16-F10 cells were subcutaneously injected into the C57BL/6J mice (control group) and Mac-1 -/ -mice (experiment group), respectively. Subsequently,the survival rate, tumor volume and body weight were recorded. The proliferation and infiltration of macrophages were detected by immunohistochemistry. Results The survival rate of Mac-1 -/ - mice was significantly improved compared with the C57BL/6J mice (P ﹤0. 001). The tumor volume and body weight were remarkably decreased in the Mac-1 -/ - mice compared with the control group (P﹤0. 001). Meanwhile, the tumor cell proliferation index was decreased in the Mac-1 -/ - mice compared with the control group (P﹤0. 01). Furthermore, the infiltration of macrophages in the tumor tissues was also decreased in Mac-1 -/ - tumor mice compared with control group. Conclusions Mac-1 gene deletion can significantly suppress melanoma growth.

19.
Article in Chinese | WPRIM | ID: wpr-668259

ABSTRACT

Objective To investigate the therapeutic effects of Quercetin (QT)-loaded PLGA-TPGS nanoparticles (QPTN) on solid tumor-bearing mice with HCa-F hepatocarcinoma in vivo.Methods The model of HCa-F hepatocarcinoma solid tumor-bearing mice was established by implanting HCa-F cells into 48 mice.The mice were divided into 6 groups randomly:the negative control,empty PLGA-TPGS nanoparticles,5-Fluorouracil solutions (FS),Quercetin solutions (QTS),QT-loaded PLGA nanoparticles (QPN),and QPTN groups.Each group was treated using tail vein twice a day for 20 days;then,all mice were sacrificed.The increment tumor volumes and tumor growth inhibition rate were counted.Then,tumor specimens were prepared for hematoxylin & eosin (HE) staining and observed under a microscope.Results The results showed that the increment tumor volumes of mice in the QPTN,QPN,and FS groups were significantly smaller than that in the negative control group (P < 0.05 or P < 0.01).The tumor growth inhibition rate of the QPTN group was 59.07%,which was much higher than that of the QTS group (23.94%),the FS group (35.14%),and the QPN group (46.14%).The results of the HE staining on the tumor sections also indicated that the QPTN group showed a better therapeutic outcome compared to the other groups.Conclusion The QPTN has a better therapeutic effect on the model of solid tumor using HCa-F cells-bearing mice than the QPN,QTS,and FS.

20.
Article in Chinese | WPRIM | ID: wpr-661328

ABSTRACT

Cancer cell metabolic reprogramming is a highly significant feature in tumor development and progression.This process is an extension of aerobic glycolysis(i.e.,Warburg effect).The metabolic pattern,such as that of glycolysis,oxidative phosphorylation, amino acid metabolism,fatty acid metabolism,and nucleic acid metabolism,is altered significantly during cell carcinogenesis.Fatty ac-id metabolism is required for energy storage,membrane proliferation,and signaling molecule generation.Thus,studying the mecha-nism of de novo fatty acid synthesis and its relationship with the development and progression of tumor,as well as the use and target-ing of the key enzyme in this metabolic pathway,is vital for the diagnosis,prevention,and treatment of cancer.Herein,we provide a brief review of metabolic reprogramming in cancer cells.We focus on the pathways of de novo fatty acid synthesis during the develop-ment and progression of tumor.

SELECTION OF CITATIONS
SEARCH DETAIL