Natural compounds targeting glycolysis as promising therapeutics for gastric cancer: A review

Zhao, Maoyuan; Feng, Wei; Sun, Guangwei; Wen, Yueqiang; Xiang, Juyi; Su, Fangting; Zhan, Lu; Nian, Qing; Chen, Yu; Zeng, Jinhao

doi:10.3389/fphar.2022.1004383

Cited by 9 publications

(5 citation statements)

References 197 publications

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“…In recent years, there have been notable advancements in targeted cancer therapies. These therapies employ drugs that specifically target and inhibit molecules or signaling pathways associated with cancer cells, such as tyrosine kinase inhibitors and monoclonal antibodies [ 5 ]. Despite the progress made, the diverse subtypes of cancer and the development of drug resistance pose challenges in achieving comprehensive cancer inhibition or cure using a single drug.…”

Section: Introductionmentioning

confidence: 99%

Proteome-wide mendelian randomization study implicates therapeutic targets in common cancers

Ren,

Jin,

Liu

et al. 2023

J Transl Med

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Background The interest in targeted cancer therapies has been growing rapidly. While numerous cancer biomarkers and targeted treatment strategies have been developed and employed, there are still significant limitations and challenges in the early diagnosis and targeted treatment of cancers. Accordingly, there is an urgent need to identify novel targets and develop new targeted drugs. Methods The study was conducted using combined cis-Mendelian randomization (cis-MR) and colocalization analysis. We analyzed data from 732 plasma proteins to identify potential drug targets associated with eight site-specific cancers. These findings were further validated using the UK Biobank dataset. Then, a protein–protein interaction network was also constructed to examine the interplay between the identified proteins and the targets of existing cancer medications. Results This MR analysis revealed associations between five plasma proteins and prostate cancer, five with breast cancer, and three with lung cancer. Subsequently, these proteins were classified into four distinct target groups, with a focus on tier 1 and 2 targets due to their higher potential to become drug targets. Our study indicatied that genetically predicted KDELC2 (OR: 0.89, 95% CI 0.86–0.93) and TNFRSF10B (OR: 0.74, 95% CI 0.65–0.83) are inversely associated with prostate cancer. Furthermore, we observed an inverse association between CPNE1 (OR: 0.96, 95% CI 0.94–0.98) and breast cancer, while PDIA3 (OR: 1.19, 95% CI 1.10–1.30) were found to be associated with the risk of breast cancer. In addition, we also propose that SPINT2 (OR: 1.05, 95% CI 1.03–1.06), GSTP1 (OR: 0.82, 95% CI 0.74–0.90), and CTSS (OR: 0.91, 95% CI 0.88–0.95) may serve as potential therapeutic targets in prostate cancer. Similarly, GDI2 (OR: 0.85, 95% CI 0.80–0.91), ISLR2 (OR: 0.87, 95% CI 0.82–0.93), and CTSF (OR: 1.14, 95% CI 1.08–1.21) could potentially be targets for breast cancer. Additionally, we identified SFTPB (OR: 0.93, 95% CI 0.91–0.95), ICAM5 (OR: 0.95, 95% CI 0.93–0.97), and FLRT3 (OR: 1.10, 95% CI 1.05–1.15) as potential targets for lung cancer. Notably, TNFRSF10B, GSTP1, and PDIA3 were found to interact with the target proteins of current medications used in prostate or breast cancer treatment. Conclusions This comprehensive analysis has highlighted thirteen plasma proteins with potential roles in three site-specific cancers. Continued research in this area may reveal their therapeutic potential, particularly KDELC2, TNFRSF10B, CPNE1, and PDIA3, paving the way for more effective cancer treatments.

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Section: Introductionmentioning

confidence: 99%

Proteome-wide mendelian randomization study implicates therapeutic targets in common cancers

Ren,

Jin,

Liu

et al. 2023

J Transl Med

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“…Targeting CEMIP emerges as a promising therapeutic strategy for gastric cancer, considering its role in promoting tumor progression, metastasis, and its involvement in multiple signaling pathways. Natural compounds like curcumin, resveratrol, and quercetin have demonstrated the suppression of CEMIP expression and activity in gastric cancer cells, inhibiting glycolysis, migration, and invasion ( Zhao et al, 2022 ) . Furthermore, angiogenesis-targeted therapies like ramucirumab and apatinib may indirectly modulate CEMIP levels by influencing the tumor microenvironment ( Nakayama & Takahari, 2023 ).…”

Section: Survey Methodologymentioning

confidence: 99%

The role of CEMIP in cancers and its transcriptional and post-transcriptional regulation

Guo,

Chen

et al. 2024

PeerJ

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CEMIP is a protein known for inducing cell migration and binding to hyaluronic acid. Functioning as a hyaluronidase, CEMIP primarily facilitates the breakdown of the extracellular matrix component, hyaluronic acid, thereby regulating various signaling pathways. Recent evidence has highlighted the significant role of CEMIP in different cancers, associating it with diverse pathological states. While identified as a biomarker for several diseases, CEMIP’s mechanism in cancer seems distinct. Accumulating data suggests that CEMIP expression is triggered by chemical modifications to itself and other influencing factors. Transcriptionally, chemical alterations to the CEMIP promoter and involvement of transcription factors such as AP-1, HIF, and NF-κB regulate CEMIP levels. Similarly, specific miRNAs have been found to post-transcriptionally regulate CEMIP. This review provides a comprehensive summary of CEMIP’s role in various cancers and explores how both transcriptional and post-transcriptional mechanisms control its expression.

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“…Poor oral bioavailability is a problem associated with several natural products. Herbal nanomedicine (HNM) is a drug particle with a diameter of 10–200 nm (Zhao et al, 2022). These are formed by combining herbal ingredients with nanoparticles through nanotechnology.…”

Section: Critical Considerationsmentioning

confidence: 99%

Targeting lipid metabolism with natural products: A novel strategy for gastrointestinal cancer therapy

Guo

Zhang

Zhao

et al. 2023

Phytotherapy Research

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Gastrointestinal cancer (GIC), including gastric cancer and colorectal cancer, is a common malignant tumor originating from gastrointestinal epithelial cells. Although the pathogenesis of GIC remains unclear, aberrant lipid metabolism has emerged as a hallmark of cancer. Several enzymes, proteins, and transcription factors are involved in lipid metabolism reprogramming in GIC, and their abnormal expression can promote lipid synthesis and accumulation of lipid droplets through numerous mechanisms, thereby affecting the growth, proliferation, and metastasis of GIC cells.Studies show that some natural compounds, including flavonoids, alkaloids, and saponins, can inhibit the de novo synthesis of lipids in GIC, reduce the level of lipid accumulation, and subsequently, inhibit the occurrence and development of GIC by regulating Sterol regulatory element-binding protein 1 (SREBP-1), adenosine monophosphate-activated protein kinase (AMPK), 3-hydroxy-3-methylglutarylcoenzyme A reductase (HMGCR), phosphatidylinositol-3-kinase/Akt and the mammalian target of rapamycin PI3K/Akt/mTOR, amongst other targets and pathways. Therefore, targeting tumor lipid metabolism is the focus of anti-gastrointestinal tumor therapy. Although most natural products require further high-quality studies to firmly establish their clinical efficacy, we review the potential of natural products in the treatment of GIC and summarize the application prospect of lipid metabolism as a new target for the treatment of GIC, hoping to provide a reference for drug development for gastrointestinal tumors.

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Natural compounds targeting glycolysis as promising therapeutics for gastric cancer: A review

Cited by 9 publications

References 197 publications

Proteome-wide mendelian randomization study implicates therapeutic targets in common cancers

Proteome-wide mendelian randomization study implicates therapeutic targets in common cancers

The role of CEMIP in cancers and its transcriptional and post-transcriptional regulation

Targeting lipid metabolism with natural products: A novel strategy for gastrointestinal cancer therapy

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