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  • 1
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    Abstract 4618: mTOR signaling complex can be targeted using Torin2 in colorectal cancer to induce efficient apoptosis
    American Association for Cancer Research (AACR) ; 2016
    In:  Cancer Research Vol. 76, No. 14_Supplement ( 2016-07-15), p. 4618-4618
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 76, No. 14_Supplement ( 2016-07-15), p. 4618-4618
    Abstract: Colorectal cancer (CRC) is the third most common cancer in the world and the 4th most common cause of cancer related death. Despite the considerable advances in awareness, diagnosis and modern therapeutic strategies, the incidence of CRC is increasing in the Middle Eastern population. In order to explore the molecular cause of increasing incidence of CRC in this region, we sought to evaluate the role of mammalian target of rapamycin (mTOR) survival pathway in CRC of this region. mTOR; a component of the phosphatidylinositol 3-kinase (PI3K) cell survival pathway, is known to play an important role in the regulation of many cellular activities leading to cell growth and proliferation through the formation of its two complexes mTORC1 and mTORC2. We therefore examined the expression of mTOR in 700 Saudi CRC cases by immunohistochemistry in a tissue microarray format and found that mTORC1 and mTORC2 were activated in 43.4% (294/677) and 46.2% (313/677) of cases respectively. mTORC1 activation was found to be significantly associated with Ki67 and mTORC2. In addition, mTORC2 activation was also found to be directly associated with their downstream target; p-AKT. In vitro, we found that treatment with a second generation mTOR inhibitor, Torin2 led to inhibition of cell viability and induction of apoptosis via inactivation of mTORC1 and mTORC2 in majority of CRC cell lines. Inactivation of mTORC1 and mTORC2 following Torin2 treatment also led to dephosphorylation of mTOR downstream targets; P70S6, 4E-BP1, AKT and BAD. Interestingly, one CRC cell line; HT29 that had over-activation of mTORC2 was found to be resistant to Torin2 treatment suggesting that increased activation of mTORC2 confers resistance to Torin2 treatment. As our clinical data demonstrated a significant association between mTORC2 over-expression and activation of AKT in clinical CRC samples, we synergistically targeted HT29 cells with combination of sub-optimal doses of PI3-kinase/AKT inhibitor; LY294002 in combination with Torin2. Our data showed that combination of Torin2 and LY294002 synergistically induced apoptosis in HT29 cells via inactivation of mTORC2 and AKT. These data highlight the utility of targeting mTOR signaling complex using second generation mTOR inhibitors such as Torin2 alone or in combination with other inhibitors such as LY294002 or chemotherapeutic agents to effectively treat these aggressive subgroups of CRC with over-activation of mTOR and AKT simultaneously. Citation Format: Saeeda O. Ahmed, Maqbool Ahmed, Abdul K. Siraj, Shaham Beg, Saravanan Thangavel, Nasser Al-Sanea, Fouad Al-Dayel, Azhar R. Hussain, Khawla S. Al-Kuraya. mTOR signaling complex can be targeted using Torin2 in colorectal cancer to induce efficient apoptosis. [abstract] . In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 4618.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2016-4618
    RVK:
    XA 36000
    RVK:
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2016
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  • 2
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    Abstract 4775: Role of FoxM1 survival pathway in primary effusion lymphoma cells
    American Association for Cancer Research (AACR) ; 2011
    In:  Cancer Research Vol. 71, No. 8_Supplement ( 2011-04-15), p. 4775-4775
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 8_Supplement ( 2011-04-15), p. 4775-4775
    Abstract: Primary effusion lymphoma (PEL) is associated with Kaposi sarcoma herpesvirus (KSHV) but its pathogenesis is poorly understood. Many KSHV-associated products can deregulate cellular pathways commonly targeted in cancer. The clinical features and natural history of PELs differ greatly from those observed in other lymphomas. The failure to improve outcomes with treatment intensification indicates the need for the introduction of new therapeutic options. Forkhead Box M1 (FoxM1) is a transcription factor that regulates the expression of a number of genes that are involved in cell cycle regulation and metastasis. Over-expression of FoxM1 has been shown in a variety of cancer however its role has not been fully elucidated in PELs. We found that FoxM1 is constitutively expressed in PELs and treatment of PELs with thiostrepton; a specific inhibitor of FoxM1 inhibits cell viability and induces apoptosis in a dose dependent manner. In addition, thiostrepton treatment also efficiently blocks formation of colonies on agarose plates as well as inhibits cell invasion and migration of PEL cell. Thiostrepton treatment causes down-regulation of FoxM1, MMP-2 and MMP-9 in PEL cells leading to activation of the intrinsic apoptotic pathway. Thiostrepton treatment causes conformational changes of Bax protein, leading to loss of mitochondrial membrane potential and release of cytochrome c to the cytosole. This leads to activation of caspase-9, caspase-3, and polyadenosin-5’-diphosphate-ribose polymerase (PARP) cleavage leading to caspase-dependent apoptosis. Altogether, this data demonstrates the possible role of FoxM1 in pathogenesis of PELs and raise the possibility that incorporation of thiostrepton in treatment regimens for primary effusion lymphomas may improve the overall survival of patients suffering from this malignancy. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4775. doi:10.1158/1538-7445.AM2011-4775
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2011-4775
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
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    detail.hit.zdb_id: 410466-3
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  • 3
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    Abstract 170: Thymoquinone-mediated suppression of NF- αB activity causes inhibition of cell viability and induces apoptosis in activated B-cell sub-type of diffuse large B-cell lymphoma
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Research Vol. 72, No. 8_Supplement ( 2012-04-15), p. 170-170
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 8_Supplement ( 2012-04-15), p. 170-170
    Abstract: Diffuse Large B-cell Lymphoma (DLBCL) is the most common lymphoid malignancy and constitutes approximately 40% of all cases of non-Hodgkin's lymphoma (NHL). Despite improvement in treatment protocols, a large number of DLBCL cases remain refractory to treatment. DLBCL can be further classified as three distinct subtypes: germinal center B cell-like (GCB)-, activated B cell-like (ABC)-, and primary mediastinal B-cell lymphoma (PMBL). ABC DLBCL has a worse survival after upfront chemotherapy and is characterized by constitutive activation of the anti-apoptotic nuclear factor-kappa B (NF-κB) pathway. Yet the implication of NF-κB inhibition in ABC DLBCL need to be further elucidated. We have previously shown that Thymoquinone (TQ), a natural compound isolated from Nigella sativa, induces growth inhibition and induces apoptosis in several NHL cell lines. However its role in inhibition of growth and apoptosis has not been fully elucidated in ABC sub-type of DLBCL cell lines. We found that TQ treatment inhibits cell viability and induces apoptosis in a dose dependent manner in various ABC cell lines. Further more, we found that TQ treatment causes inactivation of IκBα and consequently inhibits NF-κB activity by decreasing the expression of p65 subunit of NF-κB in the nuclear compartment of ABC cell lines. In-activation of NF-κB survival pathway leads to induction of apoptosis via the mitochondrial apoptotic pathway initiated by conformational changes in the Bax protein leading to changes in the mitochondrial membrane potential and release of cytochrome c in the cytosole. Once cytochrome c is released, it leads to activation and cleavage of caspases-9 and -3 and cleavage of PARP. This leads to caspase dependent apoptosis in ABC cell lines. In addition, we also found that TQ treatment causes up-regulation of death receptor 5 (DR5), an important and essential receptor for tumor necrosis factor related apoptosis inducing ligand (TRAIL). However, up-regulation of DR5 does not play a role in TQ-induced apoptosis in ABC cell lines. Interestingly, combination of sub-toxic doses of TQ and TRAIL induces efficient significant apoptosis in ABC cell lines. These data show that TQ can be used alone or in combination with TRAIL to induce apoptosis in these aggressive sub-types of DLBCL and may play an important role in the management of DLBCL in the future. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 170. doi:1538-7445.AM2012-170
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2012-170
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
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  • 4
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    Resveratrol Suppresses Constitutive Activation of AKT via Generation of ROS and Induces Apoptosis in Diffuse Large B Cell Lymphoma Cell Lines
    Public Library of Science (PLoS) ; 2011
    In:  PLoS ONE Vol. 6, No. 9 ( 2011-9-12), p. e24703-
    Details
    In: PLoS ONE, Public Library of Science (PLoS), Vol. 6, No. 9 ( 2011-9-12), p. e24703-
    Type of Medium: Online Resource
    ISSN: 1932-6203
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    DOI: 10.1371/journal.pone.0024703
    DOI: 10.1371/journal.pone.0024703.g001
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    DOI: 10.1371/journal.pone.0024703.g007
    DOI: 10.1371/journal.pone.0024703.s001
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    DOI: 10.1371/journal.pone.0024703.s003
    Language: English
    Publisher: Public Library of Science (PLoS)
    Publication Date: 2011
    detail.hit.zdb_id: 2267670-3
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  • 5
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    Cross-Talk between NFkB and the PI3-Kinase/AKT Pathway Can Be Targeted in Primary Effusion Lymphoma (PEL) Cell Lines for Efficient Apoptosis
    Public Library of Science (PLoS) ; 2012
    In:  PLoS ONE Vol. 7, No. 6 ( 2012-6-29), p. e39945-
    Details
    In: PLoS ONE, Public Library of Science (PLoS), Vol. 7, No. 6 ( 2012-6-29), p. e39945-
    Type of Medium: Online Resource
    ISSN: 1932-6203
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    DOI: 10.1371/journal.pone.0039945
    DOI: 10.1371/journal.pone.0039945.g001
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    DOI: 10.1371/journal.pone.0039945.g006
    DOI: 10.1371/journal.pone.0039945.t001
    DOI: 10.1371/journal.pone.0039945.s001
    DOI: 10.1371/journal.pone.0039945.s002
    DOI: 10.1371/journal.pone.0039945.s003
    Language: English
    Publisher: Public Library of Science (PLoS)
    Publication Date: 2012
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  • 6
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    Thymoquinone suppresses growth and induces apoptosis via generation of reactive oxygen species in primary effusion lymphoma
    Elsevier BV ; 2011
    In:  Free Radical Biology and Medicine Vol. 50, No. 8 ( 2011-4), p. 978-987
    Details
    In: Free Radical Biology and Medicine, Elsevier BV, Vol. 50, No. 8 ( 2011-4), p. 978-987
    Type of Medium: Online Resource
    ISSN: 0891-5849
    URL: Article
    DOI: 10.1016/j.freeradbiomed.2010.12.034
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2011
    detail.hit.zdb_id: 1483653-1
    SSG: 12
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  • 7
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    High prevalence of mTOR complex activity can be targeted using Torin2 in papillary thyroid carcinoma
    Oxford University Press (OUP) ; 2014
    In:  Carcinogenesis Vol. 35, No. 7 ( 2014-7), p. 1564-1572
    Details
    In: Carcinogenesis, Oxford University Press (OUP), Vol. 35, No. 7 ( 2014-7), p. 1564-1572
    Type of Medium: Online Resource
    ISSN: 1460-2180 , 0143-3334
    URL: Article
    DOI: 10.1093/carcin/bgu051
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2014
    detail.hit.zdb_id: 1474206-8
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  • 8
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    Abstract 1492: FoxM1 expression and its association with matrix metalloproteinases in diffuse large B-cell lymphoma
    American Association for Cancer Research (AACR) ; 2011
    In:  Cancer Research Vol. 71, No. 8_Supplement ( 2011-04-15), p. 1492-1492
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 8_Supplement ( 2011-04-15), p. 1492-1492
    Abstract: Forkhead Box M1 (FoxM1) has been shown to play a critical role in pathogenesis of various malignancies however its role in lymphoid malignancies is not fully elucidated. Therefore, in this study, we first investigated the role of FoxM1 in a large series of DLBCL tissues in a tissue micro array (TMA) format by Immunohistochemistry (IHC). We then followed this with in vitro studies on DLBCL cell lines using either pharmacological inhibitors of FoxM1 or siRNA knock down strategy. Using IHC, FoxM1 was detected in 84.6% of DLBCL tumors. FoxM1 expression was found to be significantly associated with early stage (p=0.0149), germinal centre phenotype (p=0.0126) and high proliferative tumor marker Ki67 (p & lt;0.0001). In addition, FoxM1 expression was also significantly associated with expression of SKP2 (p & lt;0.0001) and inversely associated with p27 expression (0.0215). Metalloproteinases, such as MMP-2 and MMP-9 play an important role in invasion and migration of cancer cells were also found to be significantly associated with expression of FoxM1 (p=0.0008 and p=0.0002) respectively. Our in vitro studies showed that treatment of DLBCL cell lines with thiostrepton, a specific inhibitor of FoxM1 inhibited cell proliferation, invasion and migration of DLBCL cells and induced apoptosis in a dose dependent manner. Inhibition of FoxM1 led to down-regulation of MMP-2, MMP-9 and SKP2 expression while the expression of p27 was up-regulated in DLBCL cells. Similar results were obtained using siRNA targeted against FoxM1. Furthermore, treatment of DLBCL cells with thiostrepton caused a dose dependent apoptosis in all DLBCL cell lines used in the study. On dissecting the apoptotic pathway, we found that thiostrepton induced its apoptotic effect via the mitochondrial pathway and activation of caspases. Finally, treatment of DLBCL cells with thiostrepton down-regulated the expression of XIAP, cIAP1 and Survivin. Altogether, these results suggest that FoxM1 signaling contribute in pathogenesis of germinal centre subtype of DLBCL and may serve as useful molecular biomarker and potential therapeutic target. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1492. doi:10.1158/1538-7445.AM2011-1492
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2011-1492
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 9
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    Abstract 4778: Resveratrol suppresses constitutive activation of AKT via generation of reactive oxygen species and induces apoptosis in diffuse large B cell lymphoma cell lines
    American Association for Cancer Research (AACR) ; 2011
    In:  Cancer Research Vol. 71, No. 8_Supplement ( 2011-04-15), p. 4778-4778
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 8_Supplement ( 2011-04-15), p. 4778-4778
    Abstract: We have recently shown that deregulation PI3-kinase/AKT survival pathway plays an important role in the pathogenesis of diffuse large B cell lymphoma (DLBCL). In an attempt to identify newer agents that can be utilized to target these deregulated pathways, we found that Resveratrol (trans-3,4′, 5-trihydroxystilbene) is a naturally occurring polyphenolic compound that has an antioxidant and chemopreventive effects on various cancer cells. In the current investigation, we therefore investigated the role of resveratrol-mediated chemopreventive effect on various DLBCL cell lines. Resveratrol caused a dose dependent inhibition of cell viability in DBCL cell lines. To see whether this inhibition was due to cell cycle arrest or apoptosis, we found that resveratrol induced apoptosis in all DLBCL cell lines. We next investigated the action of resveratrol on PI3-kinase/AKT pathway and found that resveratrol treatment resulted in inhibition of constitutively activated AKT and its downstream targets, p-FOXO1, p-GSK3 and p-Bad via generation of reactive oxygen species (ROS). Inactivation of Bad led to conformational changes in Bax protein causing loss of mitochondrial membrane potential and release of cytochrome c to the cytosol. This led to activation of caspase-9, caspase-3, and poly-(ADP)-ribose polymerase cleavage leading to caspase-dependent apoptosis. In addition, resveratrol treatment of DLBCL cell lines also caused ROS dependent upregulation of DR5; however, this up-regulation did not result in apoptosis. Finally, co-treatment of DLBCL with sub-toxic doses of TRAIL and resveratrol induced efficient apoptosis. Altogether, these data suggest a novel function for resveratrol, acting as a suppressor of AKT/PKB pathway via generation of ROS in DLBCL cells, and raise the possibility that this agent may have a future therapeutic role in DLBCL and possibly other malignancies with constitutive activation of the AKT/PKB pathway either alone or in combination with other chemotherapeutic agents. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4778. doi:10.1158/1538-7445.AM2011-4778
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2011-4778
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
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  • 10
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    Abstract 4045: c-Met inhibition synergistically enhances death receptor-induced apoptosis via upregulation of DR5 in papillary thyroid cancer
    American Association for Cancer Research (AACR) ; 2011
    In:  Cancer Research Vol. 71, No. 8_Supplement ( 2011-04-15), p. 4045-4045
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 8_Supplement ( 2011-04-15), p. 4045-4045
    Abstract: The Met receptor tyrosine kinase and its ligand, hepatocyte growth factor (HGF), are overexpressed and/or activated in variety of human malignancies. Previously we have shown that c-Met was overexpressed in Middle Eastern Papillary Thyroid Cancer (PTC) and significantly associated with poor prognoses. In this study, we investigated the functional link between c-Met/AKT signaling pathway and Dearth Receptor 5 (DR5) in a large cohort of PTC patient samples, a panel of PTC cell lines, and xenografts in a NUDE mouse model by using tissue microarray, MTT, flow cytometry and DNA fragmentation assays and western blotting. Immunohistochemistry staining showed a significant association of p-Met with DR5 in PTC patient samples. The PHA665752, an inhibitor of c-met tyrosine kinase, inhibited cell proliferation and induced apoptosis in a dose dependent manner in all cell lines studied. PHA665752 treatment resulted in dephosphorylation of c-Met, AKT and its downstream effector molecules FOXO1, GSK-3 and pBad. Additionally, treatment of PTC cell lines with PHA665752 resulted in activation of caspases-9 and 3, cleavage PARP and apoptosis. Moreover, HGF, a ligand of c-Met, stimulated the growth of all PTC cell lines via activation of c-MET and AKT. In addition, pre-treatment of PTC cell line with PHA665752 abrogated the HGF stimulated growth and activation of c-met and AKT further suggesting the critical role of c-met and AKT pathway in PTC pathogenesis. Furthermore, c-Met inhibitor PHA665752 up-regulated DR5 expression in PTC cell line cells, and synergistically potentiated death receptor-induced apoptosis with TRAIL. Finally, co-treatment with PHA665752 and TRAIL causes more pronounced effect on PTC xenograft tumor growth in NUDE mice. Our data suggest that c-Met/HGF pathway may be a potential target for therapeutic intervention for treatment of PTC with c-Met inhibitor alone or in combination of conventionally therapeutic agents. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4045. doi:10.1158/1538-7445.AM2011-4045
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2011-4045
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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