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| Lipid peroxidation is a chain reaction process in which free radicals (often reactive oxygen species, or ROS) attack lipids containing carbon-carbon double bonds, especially polyunsaturated fatty acids. This attack results in the formation of lipid radicals, peroxides, and subsequent breakdown products. Lipid peroxidation can cause damage to cell membranes, leading to increased permeability and disruption of cellular functions. This damage can initiate a cascade of events that may contribute to carcinogenesis. The byproducts of lipid peroxidation, such as malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE), can form adducts with DNA, leading to mutations. These mutations can disrupt normal cellular processes and contribute to the development of cancer. Lipid peroxidation damages cell membranes, disrupts cellular functions, and can trigger inflammatory responses. It is a marker of oxidative stress and is implicated in many chronic diseases. Negative Prognostic Indicator: In many cancers, high levels of lipid phosphates, particularly S1P, are associated with poor prognosis, indicating a more aggressive tumor phenotype and potential resistance to therapy. Mixed Evidence: The prognostic significance of lipid phosphates can vary by cancer type, with some studies showing that their expression may not always correlate with adverse outcomes. |
| Cyclooxygenase (COX)-2 overexpression has been noted in various cancers.
PI3Ks/AKT pathways are over-activated in several types of cancers. EGFR altered activity has been noted in various pathological conditions. However, its regulation is an important step in the inhibition of cancer. In this regard, EGCG shows a pivotal role in the inhibition of EGFR activity. Activating protein-1 transcription factor has been associated with pathogenesis including cancer. Activation of the sonic hedgehog (Shh) pathway is required for the growth of numerous tissues and organs and recent evidence indicates that this pathway is often recruited to stimulate growth of cancer stem cells (CSCs) and to orchestrate the reprogramming of cancer cells via epithelial mesenchymal transition (EMT). Increased expression of Nanog has been associated with the aggressive nature of certain cancers, highlighting its role in promoting cancer stem cell characteristics. The aberrant hedgehog (Hh)/GLI signaling pathway causes the formation and progression of a variety of tumors. The process of cell apoptosis is often accompanied by the destruction of mitochondrial transmembrane potential, which is widely regarded as one of the earliest events in the process of cell apoptosis. Human malignancies frequently exhibit mutations in the TGF-β pathway, and overactivation of this system is linked to tumor growth by promoting angiogenesis and inhibiting the innate and adaptive antitumor immune responses50. Several studies have demonstrated that high cyclin D1 expression was observed in cancers including breast, lung, prostate, lymph node and colorectal cancers [23–25]. The oncogene c-myc, which is frequently over-expressed in cancer cells, is involved in the transactivation of most of the glycolytic enzymes including lactate dehydrogenase A (LDHA) and the glucose transporter GLUT1 [51,52]. Thus, c-myc activation is a likely candidate to promote the enhanced glucose uptake and lactate release in the proliferating cancer cell. Vimentin is overexpressed in various epithelial cancers, including prostate cancer, gastrointestinal tumors, tumors of the central nervous system, breast cancer, malignant melanoma, and lung cancer. Vimentin’s overexpression in cancer correlates well with accelerated tumor growth, invasion, and poor prognosis; however, the role of vimentin in cancer progression remains obscure. Heat shock proteins (HSPs) are normally induced under environmental stress to serve as chaperones for maintenance of correct protein folding but they are often overexpressed in many cancers, including breast cancer. Since NQO1 is highly expressed in many solid tumors, including via upregulation of Nrf2, the design of compounds activated by NQO1 and NQO1-targeted drug delivery have been active areas of research. Since increased Nrf2 gene expression is one of the main mechanisms of cancer cells in resisting chemotherapeutic drugs and survival in oxidative conditions; finding compounds with the ability to suppress Nrf2 gene expression with minimum side effects can be considered an important strategy for increasing the sensitivity of cancer cells to chemotherapy. Overexpression of c-met stimulates proliferation, migration and invasion in various types of cancer including prostate cancer. Overexpression of TGFα and EGFR by many carcinomas correlates with the development of cancer metastasis, resistance to chemotherapy and poor prognosis. More than 50% of human cancers have a mutated nonfunctional p53. |
| 4549- | AgNPs, | Silver nanoparticles: Synthesis, medical applications and biosafety |
| - | Review, | Var, | NA | - | Review, | Diabetic, | NA |
| 3541- | ALA, | Insights on alpha lipoic and dihydrolipoic acids as promising scavengers of oxidative stress and possible chelators in mercury toxicology |
| - | Review, | Var, | NA |
| 3387- | ART/DHA, | Ferroptosis: A New Research Direction of Artemisinin and Its Derivatives in Anti-Cancer Treatment |
| - | Review, | Var, | NA |
| 3396- | ART/DHA, | Progress on the study of the anticancer effects of artesunate |
| - | Review, | Var, | NA |
| 5378- | ART/DHA, | Natural Agents Modulating Ferroptosis in Cancer: Molecular Pathways and Therapeutic Perspectives |
| - | Review, | Var, | NA |
| 3160- | Ash, | Withaferin A: A Pleiotropic Anticancer Agent from the Indian Medicinal Plant Withania somnifera (L.) Dunal |
| - | Review, | Var, | NA |
| 2737- | BetA, | Multiple molecular targets in breast cancer therapy by betulinic acid |
| - | Review, | Var, | NA |
| 5751- | CA, | Potential Therapeutic Implications of Caffeic Acid in Cancer Signaling: Past, Present, and Future |
| - | Review, | Var, | NA |
| 5859- | CAP, | Are We Ready to Recommend Capsaicin for Disorders Other Than Neuropathic Pain? |
| - | Review, | Var, | NA |
| 5994- | Chit, | Anticancer Activity of Chitosan, Chitosan Derivatives, and Their Mechanism of Action |
| - | Review, | Var, | NA |
| 2781- | CHr, | PBG, | Chrysin a promising anticancer agent: recent perspectives |
| - | Review, | Var, | NA |
| 2785- | CHr, | Emerging cellular and molecular mechanisms underlying anticancer indications of chrysin |
| - | Review, | Var, | NA |
| 2315- | Citrate, | Why and how citrate may sensitize malignant tumors to immunotherapy |
| - | Review, | Var, | NA |
| 1810- | dietKeto, | Oxy, | The Ketogenic Diet and Hyperbaric Oxygen Therapy Prolong Survival in Mice with Systemic Metastatic Cancer |
| - | in-vivo, | Var, | NA |
| 5048- | erastin, | How erastin assassinates cells by ferroptosis revealed |
| - | Review, | Var, | NA |
| 1656- | FA, | Ferulic Acid: A Natural Phenol That Inhibits Neoplastic Events through Modulation of Oncogenic Signaling |
| - | Review, | Var, | NA |
| 5113- | JG, | Juglone in Oxidative Stress and Cell Signaling |
| - | Review, | Var, | NA | - | Review, | AD, | NA |
| 1664- | PBG, | Anticancer Activity of Propolis and Its Compounds |
| - | Review, | Var, | NA |
| 4918- | PEITC, | Nutritional Sources and Anticancer Potential of Phenethyl Isothiocyanate: Molecular Mechanisms and Therapeutic Insights |
| - | Review, | Var, | NA |
| 1489- | RES, | Molecular mechanisms of resveratrol as chemo and radiosensitizer in cancer |
| - | Review, | Var, | NA |
| 4712- | Se, | Selenium and selenoproteins: key regulators of ferroptosis and therapeutic targets in cancer |
| - | Review, | Var, | NA |
| 2202- | SK, | Enhancing Tumor Therapy of Fe(III)-Shikonin Supramolecular Nanomedicine via Triple Ferroptosis Amplification |
| - | in-vitro, | Var, | NA |
| 5904- | TV, | Pharmacological Properties and Molecular Mechanisms of Thymol: Prospects for Its Therapeutic Potential and Pharmaceutical Development |
| - | Review, | Var, | NA | - | Review, | Stroke, | NA | - | Review, | Diabetic, | NA | - | Review, | Obesity, | NA | - | Review, | AD, | NA | - | Review, | Arthritis, | NA |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:26 Cells:% prod#:% Target#:453 State#:% Dir#:2
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