Potential anticancer properties of calotropis procera: An investigation on breast and colon cancer cells

Malhab, Lara J Bou; Bajbouj, Khuloud; Shehab, Naglaa Gamil; Elayoty, Salma. M.; Sinoj, Jithna; Adra, Saryia; Taneera, Jalal; Saleh, Mohamed A.; Abdel‐Rahman, Wael M.; Semreen, Mohammad H.; Alzoubi, Karem H.; Bustanji, Yasser; El‐Huneidi, Waseem; Abu‐Gharbieh, Eman

doi:10.1016/j.heliyon.2023.e16706

Cited by 7 publications

(6 citation statements)

References 40 publications

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“…Furthermore, consistent with our findings, there have been reports on the effect of C . procera extracts and cardiac glycosides in the inhibition of the expression of the PI3K/AKT/mTOR pathway in correlation to induce apoptosis cancer cells [ 22 , 49 – 53 ].…”

Section: Discussionmentioning

confidence: 99%

Combination of ethyl acetate fraction from Calotropis gigantea stem bark and sorafenib induces apoptosis in HepG2 cells

Chaisupasakul,

Pekthong,

Wangteeraprasert

et al. 2024

PLoS ONE

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The cytotoxicity of the ethyl acetate fraction of the Calotropis gigantea (L.) Dryand. (C. gigantea) stem bark extract (CGEtOAc) has been demonstrated in many types of cancers. This study examined the improved cancer therapeutic activity of sorafenib when combined with CGEtOAc in HepG2 cells. The cell viability and cell migration assays were applied in HepG2 cells treated with varying concentrations of CGEtOAc, sorafenib, and their combination. Flow cytometry was used to determine apoptosis, which corresponded with a decline in mitochondrial membrane potential and activation of DNA fragmentation. Reactive oxygen species (ROS) levels were assessed in combination with the expression of the phosphatidylinositol-3-kinase (PI3K)/ protein kinase B (Akt)/ mammalian target of rapamycin (mTOR) pathway, which was suggested for association with ROS-induced apoptosis. Combining CGEtOAc at 400 μg/mL with sorafenib at 4 μM, which were their respective half-IC50 concentrations, significantly inhibited HepG2 viability upon 24 h of exposure in comparison with the vehicle and each single treatment. Consequently, CGEtOAc when combined with sorafenib significantly diminished HepG2 migration and induced apoptosis through a mitochondrial-correlation mechanism. ROS production was speculated to be the primary mechanism of stimulating apoptosis in HepG2 cells after exposure to a combination of CGEtOAc and sorafenib, in association with PI3K/Akt/mTOR pathway suppression. Our results present valuable knowledge to support the development of anticancer regimens derived from the CGEtOAc with the chemotherapeutic agent sorafenib, both of which were administered at half-IC50, which may minimize the toxic implications of cancer treatments while improving the therapeutic effectiveness toward future medical applications.

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Section: Discussionmentioning

confidence: 99%

Combination of ethyl acetate fraction from Calotropis gigantea stem bark and sorafenib induces apoptosis in HepG2 cells

Chaisupasakul,

Pekthong,

Wangteeraprasert

et al. 2024

PLoS ONE

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“…p21 is a cyclin-dependent kinase inhibitor that functions as a checkpoint in the cell cycle. The role of HIF-1α in inducing cell cycle arrest during hypoxia varies depending on the specific context and tumor type being studied [ 30 ]. HIF-1α also plays a role in cell proliferation and survival.…”

Section: Hif-1α In Cancer: Oxygen-dependent Regulation and Tumor Prog...mentioning

confidence: 99%

“…Other strategies could also be effective in protein degradation like a nucleic acid-based strategy by using G-rich oligonucleotides that target the HIF-1α protein rather than its mRNA. Also, some natural products such as berberine allow HIF-1α degradation induction and its anti-angiogenic effects in cancer cells and in endothelial cells [ 30 , 95 , 96 , 97 ].…”

Section: Targeting Hif-1α As a Cancer Therapymentioning

confidence: 99%

Targeting Hypoxia-Inducible Factor-1 (HIF-1) in Cancer: Emerging Therapeutic Strategies and Pathway Regulation

Qannita,

Alalami,

Harb

et al. 2024

Pharmaceuticals

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Hypoxia-inducible factor-1 (HIF-1) is a key regulator for balancing oxygen in the cells. It is a transcription factor that regulates the expression of target genes involved in oxygen homeostasis in response to hypoxia. Recently, research has demonstrated the multiple roles of HIF-1 in the pathophysiology of various diseases, including cancer. It is a crucial mediator of the hypoxic response and regulator of oxygen metabolism, thus contributing to tumor development and progression. Studies showed that the expression of the HIF-1α subunit is significantly upregulated in cancer cells and promotes tumor survival by multiple mechanisms. In addition, HIF-1 has potential contributing roles in cancer progression, including cell division, survival, proliferation, angiogenesis, and metastasis. Moreover, HIF-1 has a role in regulating cellular metabolic pathways, particularly the anaerobic metabolism of glucose. Given its significant and potential roles in cancer development and progression, it has been an intriguing therapeutic target for cancer research. Several compounds targeting HIF-1-associated processes are now being used to treat different types of cancer. This review outlines emerging therapeutic strategies that target HIF-1 as well as the relevance and regulation of the HIF-1 pathways in cancer. Moreover, it addresses the employment of nanotechnology in developing these promising strategies.

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“…Natural product extracts (NPEs) represent a tremendous source of novel drugs and chemical compounds. In ancient life, NPEs were used to treat various health conditions ranging from simple headaches to a broader range of complex pathological conditions such as severe wounds, diabetes, cancer, tuberculosis, and many others ( Bustanji et al ., 2006 ; Mohammad et al ., 2013 ; Kasabri et al ., 2014 ; Motawi et al ., 2014 ; Harb et al ., 2018 ; Qasem et al ., 2020 ; Althaher et al ., 2022 ; Eldesouki et al ., 2022 ; Bou Malhab et al ., 2023 ; Tarawneh et al ., 2023 ). In the past few decades, modern medicines have overshadowed these compounds.…”

Section: Apoptotic Pathwaysmentioning

confidence: 99%

“…In the past few decades, modern medicines have overshadowed these compounds. However, nowadays, and with the emergence of new infectious agents that are drastically evolving, drug discovery organizations are directing their focus toward applying high throughput analysis to generate NPE libraries hoping to come up with potent potential therapeutic agents ( Thornburg et al ., 2018 ; Althaher et al ., 2022 ; Eldesouki et al ., 2022 ; Bou Malhab et al ., 2023 ; Tarawneh et al ., 2023 )…”

Section: Apoptotic Pathwaysmentioning

confidence: 99%

Unlocking the Therapeutic Potential of BCL-2 Associated Protein Family: Exploring BCL-2 Inhibitors in Cancer Therapy

Dakkak,

Taneera,

El-Huneidi

et al. 2024

Biomol Ther (Seoul)

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Apoptosis, programmed cell death pathway, is a vital physiological mechanism that ensures cellular homeostasis and overall cellular well-being. In the context of cancer, where evasion of apoptosis is a hallmark, the overexpression of anti-apoptotic proteins like Bcl2, Bcl-xL and Mcl-1 has been documented. Consequently, these proteins have emerged as promising targets for therapeutic interventions. The BCL-2 protein family is central to apoptosis and plays a significant importance in determining cellular fate serving as a critical determinant in this biological process. This review offers a comprehensive exploration of the BCL-2 protein family, emphasizing its dual nature. Specifically, certain members of this family promote cell survival (known as anti-apoptotic proteins), while others are involved in facilitating cell death (referred to as pro-apoptotic and BH3-only proteins). The potential of directly targeting these proteins is examined, particularly due to their involvement in conferring resistance to traditional cancer therapies. The effectiveness of such targeting strategies is also discussed, considering the tumor's propensity for anti-apoptotic pathways. Furthermore, the review highlights emerging research on combination therapies, where BCL-2 inhibitors are used synergistically with other treatments to enhance therapeutic outcomes. By understanding and manipulating the BCL-2 family and its associated pathways, we open doors to innovative and more effective cancer treatments, offering hope for resistant and aggressive cases.

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Potential anticancer properties of calotropis procera: An investigation on breast and colon cancer cells

Cited by 7 publications

References 40 publications

Combination of ethyl acetate fraction from Calotropis gigantea stem bark and sorafenib induces apoptosis in HepG2 cells

Combination of ethyl acetate fraction from Calotropis gigantea stem bark and sorafenib induces apoptosis in HepG2 cells

Targeting Hypoxia-Inducible Factor-1 (HIF-1) in Cancer: Emerging Therapeutic Strategies and Pathway Regulation

Unlocking the Therapeutic Potential of BCL-2 Associated Protein Family: Exploring BCL-2 Inhibitors in Cancer Therapy

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