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Natural anti-cancer products: insights from herbal medicine.

Herbal medicine exhibits a broad spectrum of potent anti-cancer properties, including the enhancement of tumor immune responses, reversal of multidrug resistance, regulation of autophagy and ferroptosis, as well as anti-proliferative, pro-apoptotic, and anti-metastatic effects. This review systematically explores recent advances (primarily documented since 2019) in research on key anti-cancer compounds derived from herbal medicine, such as apigenin, artemisinin, berberine, curcumin, emodin, epigallocatechin gallate (EGCG), ginsenosides, icariin, resveratrol, silibinin, triptolide, and ursolic

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… In melanoma cells, berberine induces autophagic cell death by inactivating the AKT/mTOR signaling pathway [ 224 ]. Similarly, in acute lymphoblastic leukemia cells, berberine induces autophagy and cell death by inhibiting the AKT/mTORC1 signaling pathway [ 225 ]. …

Benzyl isothiocyanate suppresses development of thyroid carcinoma by regulating both autophagy and apoptosis pathway.

Anaplastic thyroid carcinoma (ATC) is the most aggressive type of thyroid cancer, characterized by rapid growth and invasion and poor prognosis. Due to its rarity and aggressive nature, ATC is a difficult condition to treat, thus knowledge of the mechanisms underlying its progression represents important research challenges. Benzyl isothiocyanate (BITC) is a natural compound that has shown promising anticancer properties. The aim of this study was to evaluate the antitumor effect of BITC in ATC, highlighting signaling pathways involved in BITC mechanism of action. This work included in vitro a

Antimitotic drugs in the treatment of cancer.

Cancer is a complex disease since it is adaptive in such a way that it can promote proliferation and invasion by means of an overactive cell cycle and in turn cellular division which is targeted by antimitotic drugs that are highly validated chemotherapy agents. However, antimitotic drug cytotoxicity to non-tumorigenic cells and multiple cancer resistance developed in response to drugs such as taxanes and vinca alkaloids are obstacles faced in both the clinical and basic research field to date. In this review, the classes of antimitotic compounds, their mechanisms of action and cancer cell res

CXCL13 Повреждает позвоночник крови, поощряя RNF6/Sqstm1-Ubictiination.

Повреждение позвоночника крови (BSCB) приводит к нарушению иммунной микроокружающей среды в центральной нервной системе во время развития множественного склероза (MS) и экспериментального аллергического энцефаломиэлита (EAE). Тем не менее основные механизмы, связанные с повреждением барьера, по-прежнему недостаточно изучены. Здесь, анализируя белковые профили в периферической сыворотке крови, хемокин (C-X-C motif) Ligand 13 (CXCL13) был определен как возрастающий по мере развития MS и EAE. Отсутствие CXCL13 привело к снижению симптомов EAE, о чем свидетельствует сокращение числа клинических оц

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… In contrast to the protective role of autophagy in maintaining cellular homeostasis, excessive autophagy will lead to cellular metabolic imbalance and stress response disorder and ultimately induce autophagic cell death. [ 24 , 25 ] Studies have shown that autophagy is not only closely …

Effect of the specific proteasome inhibitor bortezomib on cancer-related muscle wasting.

BACKGROUND: Muscle wasting, a prominent feature of cancer cachexia, is mainly caused by sustained protein hypercatabolism. The enhanced muscle protein degradation rates rely on the activity of different proteolytic systems, although the Adenosine triphosphate (ATP)-ubiquitin-proteasome-dependent pathway and autophagy have been shown to play a pivotal role. Bortezomib is a potent reversible and selective proteasome and NF-κB inhibitor approved for the clinical use, which has been shown to be effective in preventing muscle wasting in different catabolic conditions. The aim of the present study h

Storage diseases with hypertrophic cardiomyopathy phenotype.

Never judge a book by its cover, nor assume hypertrophic cardiomyopathy (HCM) as sarcomeric, as appearances can deceive. HCM phenocopies account for a 5-10% of the cases, mainly represented by storage diseases, flagged by the increasing prevalence of senile cardiac amyloid in developing countries. Multisystemic and heterogeneous presentation of these entities is a challenge for clinicians, and time delay in diagnosis is a major concern. Promising drugs and gene-specific tailored therapies are under development, therefore, more than ever, appropriate understanding of these conditions is mandato

Mutant p53, Stabilized by Its Interplay with HSP90, Activates a Positive Feed-Back Loop Between NRF2 and p62 that Induces Chemo-Resistance to Apigenin in Pancreatic Cancer Cells.

Pancreatic cancer is one of the most aggressive cancers whose prognosis is worsened by the poor response to the current chemotherapies. In this study, we investigated the cytotoxic effect of Apigenin, against two pancreatic cell lines, namely Panc1 and PaCa44, harboring different p53 mutations. Apigenin is a flavonoid widely distributed in nature that displays anti-inflammatory and anticancer properties against a variety of cancers. Here we observed that Apigenin exerted a stronger cytotoxic effect against Panc1 cell line in comparison to PaCa44. Searching for mechanisms responsible for such d

Melanoma bone metastasis-induced osteocyte ferroptosis via the HIF1α-HMOX1 axis.

Osteocytes are the main cells in mineralized bone tissue. Elevated osteocyte apoptosis has been observed in lytic bone lesions of patients with multiple myeloma. However, their precise contribution to bone metastasis remains unclear. Here, we investigated the pathogenic mechanisms driving melanoma-induced osteocyte death. Both in vivo models and in vitro assays were combined with untargeted RNA sequencing approaches to explore the pathways governing melanoma-induced osteocyte death. We could show that ferroptosis is the primary mechanism behind osteocyte death in the context of melanoma bone m

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… Gao M Ferroptosis is an autophagic cell death process Cell Res. 2016 26 1021 1032 10.1038/cr.2016.95 27514700 PMC5034113 Gao, M. et al. Ferroptosis is an autophagic cell death process. Cell Res. 26 , 1021–1032 (2016). 27514700 10.1038/cr.2016.95 PMC5034113 46. …

Lithium: A Promising Anticancer Agent.

Lithium is a therapeutic cation used to treat bipolar disorders but also has some important features as an anti-cancer agent. In this review, we provide a general overview of lithium, from its transport into cells, to its innovative administration forms, and based on genomic, transcriptomic, and proteomic data. Lithium formulations such as lithium acetoacetate (LiAcAc), lithium chloride (LiCl), lithium citrate (Li3C6H5O7), and lithium carbonate (Li2CO3) induce apoptosis, autophagy, and inhibition of tumor growth and also participate in the regulation of tumor proliferation, tumor invasion, and

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… . | [ 21 ] Li 3 C 6 H 5 O 7 and Li 2 CO 3 particles | Hepatocellular carcinoma | Cell line HCC-29 (hepatocarcinoma) | 5 mM lithium salts | Nanosized lithium citrate mainly induced apoptosis, whereas lithium carbonate induced apoptosis and autophagic cell death. | [ 22 ] LiCl | Glioblastoma | Human TP53wt … In addition, nanosized lithium citrate induces apoptosis, whereas nanoparticles of lithium carbonate induce apoptosis and autophagic cell death of HCC cells [ 22 ]. …

An integrative review of nonobvious puzzles of cellular and molecular cardiooncology.

Oncologic patients are subjected to four major treatment types: surgery, radiotherapy, chemotherapy, and immunotherapy. All nonsurgical forms of cancer management are known to potentially violate the structural and functional integrity of the cardiovascular system. The prevalence and severity of cardiotoxicity and vascular abnormalities led to the emergence of a clinical subdiscipline, called cardiooncology. This relatively new, but rapidly expanding area of knowledge, primarily focuses on clinical observations linking the adverse effects of cancer therapy with deteriorated quality of life of

The progression of HMGB1-induced autophagy in cancer biology.

Autophagy is an important process of cellular degradation and has been proven to contribute to tumorigenesis. High-mobility group box 1 (HMGB1) is an abundant nonhistone protein that has been widely reported to play a central role in the induction of autophagy. In nucleus, HMGB1 upregulates the expression of HSP27 to induce autophagy. In cytoplasm, the Beclin-1/PI3K-III complex can be activated by HMGB1 to promote autophagy. Extracellular HMGB1 binds to the receptor for advanced glycation end products to induce autophagy. Recent studies have shown that HMGB1-induced autophagy exerts multiple f

Targeting Cancer Through Thymoquinone: From Molecular Mechanisms to Clinical Prospects.

Thymoquinone (TQ), the active compound in Nigella sativa (black seed), has shown promising effects against cancer in many laboratory studies. In this review, we explore how TQ works on different aspects of cancer, from stopping cancer cell growth and spread, to triggering cancer cell death, reducing inflammation, and helping the immune system fight back. We also highlight how TQ may overcome one of the biggest problems in cancer treatment-chemoresistance. When used together with common treatments like chemotherapy, radiation, or immunotherapy, TQ has been shown to improve their effects and red

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… In colon carcinoma (LoVo) TQ activates JNK and p38 MAPK, causing caspase-independent autophagic cell death [ 42 ]. … In glioblastoma models, TQ disrupts lysosomal membrane integrity and triggers cathepsin-B release, blocking autophagic flux and promoting non-autophagic cell death. This illustrates TQ’s context-dependent ability to redirect cell-death programs [ 43 ]. 3. …

Targeting endoplasmic reticulum stress-induced lymphatic dysfunction for mitigating bisphosphonate-related osteonecrosis.

BACKGROUND: Bisphosphonates (BPs) are the first-line treatment to stop bone resorption in diseases, including osteoporosis, Paget's disease, multiple myeloma and bone metastases of cancer. However, BPs-related osteonecrosis of the jaw (BRONJ), characterized by local inflammation and jawbone necrosis, is a severe intractable complication. The cumulative inflammatory burden often accompanies impaired lymphatic drainage, but its specific impact on BRONJ and the underlying mechanisms remain unclear. METHODS: The mouse BRONJ model was established to assess the integrity and drainage function of ly

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… As observed in BRONJ models, increased inflammation and delayed healing are associated with suppressed lymphangiogenesis. 15 Besides, ZA induces oxidative stress and altered cellular oxidative metabolism in endothelial cells, leading to autophagic cell death. 16 , 17 This process increases the expression … Zoledronate induces autophagic cell death in human umbilical vein endothelial cells via Beclin‐1 dependent pathway activation . Mol Med Rep . 2016 ; 14 ( 5 ): 4747 ‐ 4754 . 27748838 10.3892/mmr.2016.5834 PMC5102043 17 Budzinska A , Galganski L , Jarmuszkiewicz W . …

Polyphenols: Chemoprevention and therapeutic potentials in hematological malignancies.

Polyphenols are one of the largest plant-derived natural product and they play an important role in plants' defense as well as in human health and disease. A number of them are pleiotropic molecules and have been shown to regulate signaling pathways, immune response and cell growth and proliferation which all play a role in cancer development. Hematological malignancies on the other hand, are cancers of the blood. While current therapies are efficacious, they are usually expensive and with unwanted side effects. Thus, the search for newer less toxic agents. Polyphenols have been reported to po

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… A study by Guo et al. discovered that curcumin induces autophagic cell death in human Philadelphia chromosome-positive acute lymphoblastic leukemia SUP-B15 cells via activating RAF/MEK/ERK pathway ( 143 ). … Resveratrol promotes autophagic cell death in chronic myelogenous leukemia cells via JNK-mediated p62/SQSTM1 expression and AMPK activation. Cancer Res. (2010) 70:1042–52. 10.1158/0008-5472.CAN-09-3537 142. Ali Azzwali AAA, Azab AE, Alfourti AMAB. …

Proteasome inhibition paradoxically degrades gain-of-function mutant p53 R273H in NSCLC and could have therapeutic implications.

Lung cancer is the leading cause of cancer mortality. Despite therapeutic advances in recent years, new treatment strategies are needed to improve outcomes of lung cancer patients. Mutant p53 is prevalent in lung cancers and drives several hallmarks of cancer through a gain-of-function oncogenic program, and often predicts a poorer prognosis. The oncogenicity of mutant p53 is related to its stability and accumulation in cells by evading degradation by the proteasome. Therefore, destabilization of mutant p53 has been sought as a therapeutic strategy, but so far without clinical success. In this

Prevention of Anthracycline-Induced Cardiotoxicity: The Good and Bad of Current and Alternative Therapies.

Doxorubicin (Dox)-induced cardiotoxicity (DIC) remains a serious health burden, especially in developing countries. Unfortunately, the high cost of current preventative strategies has marginalized numerous cancer patients because of socio-economic factors. In addition, the efficacy of these strategies, without reducing the chemotherapeutic properties of Dox, is frequently questioned. These limitations have widened the gap and necessity for alternative medicines, like flavonoids, to be investigated. However, new therapeutics may also present their own shortcomings, ruling out the idea of "natur

Liposomal Nanoparticle Delivery of Ginkgo Flavone Glycosides Enhances SIRT1 Activation and Improves Diabetic Cardiomyopathy.

PurposeThis study aims to explore the therapeutic mechanisms of Ginkgo Flavone Glycosides (GFGs) delivered via liposomal nanoparticles in treating Diabetic Cardiomyopathy (DCM) by upregulating Sirtuin 1 (SIRT1) to restore energy metabolism and autophagy homeostasis.MethodsA DCM mouse model was employed, with groups treated with different doses of GFGs. Various evaluations, including body weight, blood glucose levels, and cardiac function, were performed. Network pharmacology, transcriptomic analysis, and molecular docking studies were conducted to elucidate the key role of SIRT1 in inhibiting

Exploring human plasma proteomic variations in mucolipidosis type IV.

Mucolipidosis IV (MLIV) is an autosomal-recessive pediatric disease that leads to motor and cognitive deficits and loss of vision. It is caused by loss of function of the lysosomal channel transient receptor potential mucolipin-1, TRPML1, and is associated with an early brain phenotype consisting of glial reactivity, hypomyelination, and lysosomal abnormalities. Although the field is approaching the first translationally relevant therapy, we currently lack a molecular signature of disease that can be used to detect therapeutic efficacy. Here, we analyzed 7,322 proteins in the plasma proteome f

Ferroptosis: a new dawn in the treatment of acute lymphoblastic leukemia.

Acute lymphoblastic leukemia poses substantial challenges in therapeutic management. As a novel form of programmed cell death, ferroptosis has emerged as a promising research direction in cancer therapy. Studies have emphasized the pivotal role of ferroptosis in ALL, indicating that targeting this pathway could provide a novel therapeutic strategy. This article systematically reviews the molecular regulatory mechanisms of ferroptosis in ALL and explores its potential clinical applications in the treatment and prognostic evaluation of the disease.

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… (PAA) inhibits T-cell acute lymphoblastic leukemia through inducing autophagic cell death and ferroptosis. Biochem Biophys Res Commun. (2022) 608:108–15. doi: 10.1016/j.bbrc.2022.03.105, PMID: 64. Simioni C, Conti I, Varano G, Brenna C, Costanzi E, Neri LM. …

Antitumoral Effects of Tricyclic Antidepressants: Beyond Neuropathic Pain Treatment.

Growing evidence shows that nerves play an active role in cancer development and progression by altering crucial molecular pathways and cell functions. Conversely, the use of neurotropic drugs, such as tricyclic antidepressants (TCAs), may modulate these molecular signals with a therapeutic purpose based on a direct antitumoral effect and beyond the TCA use to treat neuropathic pain in oncology patients. In this review, we discuss the TCAs' safety and their central effects against neuropathic pain in cancer, and the antitumoral effects of TCAs in in vitro and preclinical studies, as well as in

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… Likewise, the study by Jeon et al. suggested that imipramine exerted antitumor effects on PTEN-null U-87MG human glioma cells by inhibiting PI3K/Akt/mTOR signaling and by inducing autophagic cell death but not apoptosis [ 57 ]. … The tricyclic antidepressant imipramine induces autophagic cell death in U-87MG glioma cells. Biochem. Biophys. Res. Commun. 2011;413:311–317. doi: 10.1016/j.bbrc.2011.08.093. 58. Bielecka-Wajdman A.M., Ludyga T., Machnik G., Gołyszny M., Obuchowicz E. …