Browsing by Author "Biswas, Partha"

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A Comprehensive Analysis and Anti-Cancer Activities of Quercetin in ROS-Mediated Cancer and Cancer Stem Cells
(Scopus, 22-10-04) Biswas, Partha; Dey, Dipta; Biswas, Polash Kumar; Rahaman, Tanjim Ishraq; Saha, Shuvo; Parvez, Anwar; Khan, Dhrubo Ahmed; Lily, Nusrat Jahan; Saha, Konka; Sohel, Md; Hasan, Mohammad Mehedi; Al Azad, Salauddin; Bibi, Shabana; Hasan, Md. Nazmul; Rahmatullah, Mohammed; Chun, Jaemoo; Rahman, Md. Ataur; Kim, Bonglee
Reactive oxygen species (ROS) induce carcinogenesis by causing genetic mutations, activating oncogenes, and increasing oxidative stress, all of which affect cell proliferation, survival, and apoptosis. When compared to normal cells, cancer cells have higher levels of ROS, and they are responsible for the maintenance of the cancer phenotype; this unique feature in cancer cells may, therefore, be exploited for targeted therapy. Quercetin (QC), a plant-derived bioflavonoid, is known for its ROS scavenging properties and was recently discovered to have various antitumor properties in a variety of solid tumors. Adaptive stress responses may be induced by persistent ROS stress, allowing cancer cells to survive with high levels of ROS while maintaining cellular viability. However, large amounts of ROS make cancer cells extremely susceptible to quercetin, one of the most available dietary flavonoids. Because of the molecular and metabolic distinctions between malignant and normal cells, targeting ROS metabolism might help overcome medication resistance and achieve therapeutic selectivity while having little or no effect on normal cells. The powerful bioactivity and modulatory role of quercetin has prompted extensive research into the chemical, which has identified a number of pathways that potentially work together to prevent cancer, alongside, QC has a great number of evidences to use as a therapeutic agent in cancer stem cells. This current study has broadly demonstrated the function-mechanistic relationship of quercetin and how it regulates ROS generation to kill cancer and cancer stem cells. Here, we have revealed the regulation and production of ROS in normal cells and cancer cells with a certain signaling mechanism. We demonstrated the specific molecular mechanisms of quercetin including MAPK/ERK1/2, p53, JAK/STAT and TRAIL, AMPKα1/ASK1/p38, RAGE/PI3K/AKT/mTOR axis, HMGB1 and NF-κB, Nrf2-induced signaling pathways and certain cell cycle arrest in cancer cell death, and how they regulate the specific cancer signaling pathways as long-searched cancer therapeutics. Keywords: ROS; REDOX imbalance; carcinogenesis; malignant cells; quercetin; cancer stem cells
A Comprehensive Discussion in Vaginal Cancer Based on Mechanisms, Treatments, Risk Factors and Prevention
(Daffodil International University, 2022-07-18) Baral, Sumit Kumar; Biswas, Partha; Kaium, Md. Abu; Islam, Md. Aminul; Dey, Dipta; Saber, Md Al; Rahaman, Tanjim Ishraq; A. M.; Emran, Talha Bin; Hasan, Md. Nazmul; Jeong, Mi-Kyung; Han, Ihn; Rahman, Md. Ataur; Kim, Bonglee
Vaginal cancer is a rare and uncommon disease that is rarely discussed. Although vaginal cancer traditionally occurs in older postmenopausal women, the incidence of high-risk human papillomavirus (HPV)-induced cancers is increasing in younger women. Cervical cancer cells contain high-risk human papillomavirus (HPV) E6 and E7 proteins and inhibiting HPV gene expression leads the cells to stop proliferating and enter senescence. As E6, and E7 protein promoted the carcinogenesis mechanism, and here not only regulate the cellular degradation of P53, and pRb but also enhances the cell proliferation along with E6 protein targets the p53 for breakdown and subsequently promote the apoptotic cell death, and DNA repair inhibition, that is indispensable to the continue the lifecycle of the HPV. As a synchronous or metachronous tumor, vaginal cancer is frequently found in combination with cervical cancer. It is uncertain what causes invasive female vaginal organ cancer. HPV type 16 is the most often isolated HPV type in female vaginal organ cancers. Due to cancer’s rarity, case studies have provided the majority of etiologic findings. Many findings demonstrate that ring pessaries, chronic vaginitis, sexual behavior, birth trauma, obesity, vaginal chemical exposure, and viruses are all risk factors. Because of insufficient understanding and disease findings, we are trying to find the disease’s mechanism with the available data. We also address different risk factors, therapy at various stages, diagnosis, and management of vaginal cancer in this review.
A Comprehensive Discussion in Vaginal Cancer Based on Mechanisms, Treatments, Risk Factors and Prevention
(Daffodil International University, 2022-07-18) Baral, Sumit Kumar; Biswas, Partha; Kaium, Md. Abu; Islam, Md. Aminul; Dey, Dipta; Saber, Md Al; Rahaman, Tanjim Ishraq; M, A.; Emran, Talha Bin; Hasan, Md. Nazmul; Jeong, Mi-Kyung; Han, Ihn; Rahman, Md. Ataur; Kim, Bonglee
Vaginal cancer is a rare and uncommon disease that is rarely discussed. Although vaginal cancer traditionally occurs in older postmenopausal women, the incidence of high-risk human papillomavirus (HPV)-induced cancers is increasing in younger women. Cervical cancer cells contain high-risk human papillomavirus (HPV) E6 and E7 proteins and inhibiting HPV gene expression leads the cells to stop proliferating and enter senescence. As E6, and E7 protein promoted the carcinogenesis mechanism, and here not only regulate the cellular degradation of P53, and pRb but also enhances the cell proliferation along with E6 protein targets the p53 for breakdown and subsequently promote the apoptotic cell death, and DNA repair inhibition, that is indispensable to the continue the lifecycle of the HPV. As a synchronous or metachronous tumor, vaginal cancer is frequently found in combination with cervical cancer. It is uncertain what causes invasive female vaginal organ cancer. HPV type 16 is the most often isolated HPV type in female vaginal organ cancers. Due to cancer’s rarity, case studies have provided the majority of etiologic findings. Many findings demonstrate that ring pessaries, chronic vaginitis, sexual behavior, birth trauma, obesity, vaginal chemical exposure, and viruses are all risk factors. Because of insufficient understanding and disease findings, we are trying to find the disease’s mechanism with the available data. We also address different risk factors, therapy at various stages, diagnosis, and management of vaginal cancer in this review.
An In-Silico Identification of Potential Flavonoids against Kidney Fibrosis Targeting TGFβR-1
(Scopus, 22-11-02) Rahman, MD. Hasanur; Biswas, Partha; Dey, Dipta; Hannan, Md. Abdul; Sahabuddin, Md.; Araf, Yusha; Kwon, Youngjoo; Emran, Talha Bin; Ali, Md. Sarafat; Uddin, Md Jamal
Fibrosis is a hallmark of progressive kidney diseases. The overexpression of profibrotic cytokine, namely transforming growth factor β (TGF-β) due to excessive inflammation and tissue damage, induces kidney fibrosis. The inhibition of TGF-β signaling is markedly limited in experimental disease models. Targeting TGF-β signaling, therefore, offers a prospective strategy for the management of kidney fibrosis. Presently, the marketed drugs have numerous side effects, but plant-derived compounds are relatively safer and more cost-effective. In this study, TGFβR-1 was targeted to identify the lead compounds among flavonoids using various computational approaches, such as ADME/T (absorption, distribution, metabolism, and excretion/toxicity) analysis, molecular docking, and molecular dynamics simulation. ADME/T screening identified a total of 31 flavonoids with drug-like properties of 31 compounds, a total of 5 compounds showed a higher binding affinity to TGFβR-1, with Epicatechin, Fisetin, and Luteolin ranking at the top three (-13.58, -13.17, and -10.50 kcal/mol, respectively), which are comparable to the control drug linagliptin (-9.074 kcal/mol). The compounds also exhibited outstanding protein-ligand interactions. The molecular dynamic simulations revealed a stable interaction of these compounds with the binding site of TGFβR-1. These findings indicate that flavonoids, particularly Epicatechin, Fisetin, and Luteolin, may compete with the ligand-binding site of TGFβR-1, suggesting that these compounds can be further evaluated for the development of potential therapeutics against kidney fibrosis. Further, in-vitro and in-vivo studies are recommended to support the current findings.
he experimental significance of isorhamnetin as an effective therapeutic option for cancer: A comprehensive analysis
(Scopus, 2024-07) Biswas, Partha; Kaium, Md Abu Kaium ,; Tareq, Md Mohaimenul Islam; Tauhida, Sadia Jannat; Hossain, Md Ridoy; Siam, Labib Shahriar; Parvez, Anwar; Bibi, Shabana; Hasan, Md Hasibul; Rahman, Md Moshiur; Hosen, Delwar; Sohel, Md; Kame, Mohamed; Alamoudi, Mariam K; Daim, Mohamed M Abdel
Isorhamnetin (C16H12O7), a 3'-O-methylated derivative of quercetin from the class of flavonoids, is predominantly present in the leaves and fruits of several plants, many of which have traditionally been employed as remedies due to its diverse therapeutic activities. The objective of this in-depth analysis is to concentrate on Isorhamnetin by addressing its molecular insights as an effective anticancer compound and its synergistic activity with other anticancer drugs. The main contributors to Isorhamnetin's anti-malignant activities at the molecular level have been identified as alterations of a variety of signal transduction processes and transcriptional agents. These include ROS-mediated cell cycle arrest and apoptosis, inhibition of mTOR and P13K pathway, suppression of MEK1, PI3K, NF-κB, and Akt/ERK pathways, and inhibition of Hypoxia Inducible Factor (HIF)-1α expression. A significant number of in vitro and in vivo research studies have confirmed that it destroys cancerous cells by arresting cell cycle at the G2/M phase and S-phase, down-regulating COX-2 protein expression, PI3K, Akt, mTOR, MEK1, ERKs, and PI3K signaling pathways, and up-regulating apoptosis-induced genes (Casp3, Casp9, and Apaf1), Bax, Caspase-3, P53 gene expression and mitochondrial-dependent apoptosis pathway. Its ability to suppress malignant cells, evidence of synergistic effects, and design of drugs based on nanomedicine are also well supported to treat cancer patients effectively. Together, our findings establish a crucial foundation for understanding Isorhamnetin's underlying anti-cancer mechanism in cancer cells and reinforce the case for the requirement to assess more exact molecular signaling pathways relating to specific cancer and in vivo anti-cancer activities.
Revolutionizing Anti-Cancer Drug Discovery Against Breast Cancer and Lung Cancer by Modification of Natural Genistein
(Frontier Scientific Publishing, 2023-09-25) Akash, Shopnil; Bibi, Shabana; Biswas, Partha; Mukerjee, Nobendu; Khan, Dhrubo Ahmed; Hasan, Md. Nazmul; Sultana, Nazneen Ahmeda; Hosen, Md. Eram; Jardan, Yousef A. Bin; Nafidi, Hiba-Allah; Bourhia, Mohammed
Breast and lung cancer are two of the most lethal forms of cancer, responsible for a disproportionately high number of deaths worldwide. Both doctors and cancer patients express alarm about the rising incidence of the disease globally. Although targeted treatment has achieved enormous advancements, it is not without its drawbacks. Numerous medicines and chemotherapeutic drugs have been authorized by the FDA; nevertheless, they can be quite costly and often fall short of completely curing the condition. Therefore, this investigation has been conducted to identify a potential medication against breast and lung cancer through structural modification of genistein. Genistein is the active compound in Glycyrrhiza glabra (licorice), and it exhibits solid anticancer efficiency against various cancers, including breast cancer, lung cancer, and brain cancer. Hence, the design of its analogs with the interchange of five functional groups—COOH, NH2 and OCH3, Benzene, and NH-CH2-CH2-OH—have been employed to enhance affinities compared to primary genistein. Additionally, advanced computational studies such as PASS prediction, molecular docking, ADMET, and molecular dynamics simulation were conducted. Firstly, the PASS prediction spectrum was analyzed, revealing that the designed genistein analogs exhibit improved antineoplastic activity. In the prediction data, breast and lung cancer were selected as primary targets. Subsequently, other computational investigations were gradually conducted. The mentioned compounds have shown acceptable results for in silico ADME, AMES toxicity, and hepatotoxicity estimations, which are fundamental for their oral medication. It is noteworthy that the initial binding affinity was only −8.7 kcal/mol against the breast cancer targeted protein (PDB ID: 3HB5). However, after the modification of the functional group, when calculating the binding affinities, it becomes apparent that the binding affinities increase gradually, reaching a maximum of −11.0 and −10.0 kcal/mol. Similarly, the initial binding affinity was only −8.0 kcal/mol against lung cancer (PDB ID: 2P85), but after the addition of binding affinity, it reached −9.5 kcal/mol. Finally, a molecular dynamics simulation was conducted to study the molecular models over 100 ns and examine the stability of the docked complexes. The results indicate that the selected complexes remain highly stable throughout the 100-ns molecular dynamics simulation runs, displaying strong correlations with the binding of targeted ligands within the active site of the selected protein. It is important to further investigate and proceed to clinical or wet lab experiments to determine the practical value of the proposed compounds.
Role of T Cells in Cancer Immunotherapy: Opportunities and Challenges
(Elsevier, 2023-04-15) Ahmed, Hossain; Mahmud, Aar Rafi; Siddiquee, Mohd. Faijanur Rob; Shahriar, Asif; Biswas, Partha; Shimul, Md. Ebrahim Khalil; Ahmed, Shahlaa Zernaz; Ema, Tanzila Ismail; Rahman, Nova; Khan, Md. Arif; Mizan, Md. Furkanur Rahaman; Emran, Talha Bin
Immunotherapies boosting the immune system's ability to target cancer cells are promising for the treatment of various tumor types, yet clinical responses differ among patients and cancers. Recently, there has been increasing interest in novel cancer immunotherapy practices aimed at triggering T cell-mediated anti-tumor responses. Antigen-directed cytotoxicity mediated by T lymphocytes has become a central focal point in the battle against cancer utilizing the immune system. The molecular and cellular mechanisms involved in the actions of T lymphocytes have directed new therapeutic approaches in cancer immunotherapy, including checkpoint blockade, adoptive and chimeric antigen receptor (CAR) T cell therapy, and cancer vaccinology. This review addresses all the strategies targeting tumor pathogenesis, including metabolic pathways, to evaluate the clinical significance of current and future immunotherapies for patients with cancer, which are further engaged in T cell activation, differentiation, and response against tumors.
The Experimental Significance of Isorhamnetin as an Effective Therapeutic Option for Cancer: A Comprehensive Analysis
(IEEE, 2024-06-10) Biswas, Partha; Kaium, Md. Abu; Tareq, Md. Mohaimenul Islam; Tauhida, Sadia Jannat; Hossain, Md Ridoy; Siam, Labib Shahriar; Parvez, Anwar; Bibi, Shabana; Hasan, Md Hasibul; Rahman, Md. Moshiur; Hosen, Delwar; Siddiquee, Md. Ariful Islam; Ahmed, Nasim; Sohel, Md.; Al Azad, Salauddin; Alhadrami, Albaraa H.; Kamel, Mohamed; Alamoudi, Mariam K.; Hasan, Md. Nazmul; Abdel-Daim, Mohamed M.
Isorhamnetin (C16H12O7), a 3'-O-methylated derivative of quercetin from the class of flavonoids, is predominantly present in the leaves and fruits of several plants, many of which have traditionally been employed as remedies due to its diverse therapeutic activities. The objective of this in-depth analysis is to concentrate on Isorhamnetin by addressing its molecular insights as an effective anticancer compound and its synergistic activity with other anticancer drugs. The main contributors to Isorhamnetin's anti-malignant activities at the molecular level have been identified as alterations of a variety of signal transduction processes and transcriptional agents. These include ROS-mediated cell cycle arrest and apoptosis, inhibition of mTOR and P13K pathway, suppression of MEK1, PI3K, NF-κB, and Akt/ERK pathways, and inhibition of Hypoxia Inducible Factor (HIF)-1α expression. A significant number of in vitro and in vivo research studies have confirmed that it destroys cancerous cells by arresting cell cycle at the G2/M phase and S-phase, down-regulating COX-2 protein expression, PI3K, Akt, mTOR, MEK1, ERKs, and PI3K signaling pathways, and up-regulating apoptosis-induced genes (Casp3, Casp9, and Apaf1), Bax, Caspase-3, P53 gene expression and mitochondrial-dependent apoptosis pathway. Its ability to suppress malignant cells, evidence of synergistic effects, and design of drugs based on nanomedicine are also well supported to treat cancer patients effectively. Together, our findings establish a crucial foundation for understanding Isorhamnetin's underlying anti-cancer mechanism in cancer cells and reinforce the case for the requirement to assess more exact molecular signaling pathways relating to specific cancer and in vivo anti-cancer activities.
The Experimental Significance of Isorhamnetin as an Effective Therapeutic Option for Cancer: A Comprehensive Analysis
(Elsevier, 2024-06-10) Biswas, Partha; Kaium, Md. Abu; Tareq, Md. Mohaimenul Islam; Tauhid, Sadia Jannat; Hossain, Md Ridoy; Siam, Labib Shahriar; Parvez, Anwar; Bibi, Shabana; Hasan, Md Hasibul; Rahman, Md. Moshiur; Hosen, Delwar; Siddiquee, Md. Ariful Islam; Ahmed, Nasim; Sohel, Md.; Azad, Salauddin Al; Alhadrami, Albaraa H.; Kamel, Mohamed; Alamoudi, Mariam K.; Hasan, Md. Nazmul; Abdel-Daim, Mohamed M.
Isorhamnetin (C16H12O7), a 3'-O-methylated derivative of quercetin from the class of flavonoids, is predominantly present in the leaves and fruits of several plants, many of which have traditionally been employed as remedies due to its diverse therapeutic activities. The objective of this in-depth analysis is to concentrate on Isorhamnetin by addressing its molecular insights as an effective anticancer compound and its synergistic activity with other anticancer drugs. The main contributors to Isorhamnetin's anti-malignant activities at the molecular level have been identified as alterations of a variety of signal transduction processes and transcriptional agents. These include ROS-mediated cell cycle arrest and apoptosis, inhibition of mTOR and P13K pathway, suppression of MEK1, PI3K, NF-κB, and Akt/ERK pathways, and inhibition of Hypoxia Inducible Factor (HIF)-1α expression. A significant number of in vitro and in vivo research studies have confirmed that it destroys cancerous cells by arresting cell cycle at the G2/M phase and S-phase, down-regulating COX-2 protein expression, PI3K, Akt, mTOR, MEK1, ERKs, and PI3K signaling pathways, and up-regulating apoptosis-induced genes (Casp3, Casp9, and Apaf1), Bax, Caspase-3, P53 gene expression and mitochondrial-dependent apoptosis pathway. Its ability to suppress malignant cells, evidence of synergistic effects, and design of drugs based on nanomedicine are also well supported to treat cancer patients effectively. Together, our findings establish a crucial foundation for understanding Isorhamnetin's underlying anti-cancer mechanism in cancer cells and reinforce the case for the requirement to assess more exact molecular signaling pathways relating to specific cancer and in vivo anti-cancer activities.