S Phase

Publication Title: 
Nature

The lengths of human telomeres, which protect chromosome ends from degradation and end fusions, are crucial determinants of cell lifespan. During embryogenesis and in cancer, the telomerase enzyme counteracts telomeric DNA shortening. As shown in cancer cells, human telomerase binds the shelterin component TPP1 at telomeres during the S phase of the cell cycle, and adds ~60 nucleotides in a single round of extension, after which telomerase is turned off by unknown mechanisms.

Author(s): 
Chen, Liuh-Yow
Redon, Sophie
Lingner, Joachim
Publication Title: 
Nature

The lengths of human telomeres, which protect chromosome ends from degradation and end fusions, are crucial determinants of cell lifespan. During embryogenesis and in cancer, the telomerase enzyme counteracts telomeric DNA shortening. As shown in cancer cells, human telomerase binds the shelterin component TPP1 at telomeres during the S phase of the cell cycle, and adds ~60 nucleotides in a single round of extension, after which telomerase is turned off by unknown mechanisms.

Author(s): 
Chen, Liuh-Yow
Redon, Sophie
Lingner, Joachim
Publication Title: 
PloS One

The chronological lifespan of eukaryotic organisms is extended by the mutational inactivation of conserved growth-signaling pathways that regulate progression into and through the cell cycle. Here we show that in the budding yeast S. cerevisiae, these and other lifespan-extending conditions, including caloric restriction and osmotic stress, increase the efficiency with which nutrient-depleted cells establish or maintain a cell cycle arrest in G1.

Author(s): 
Weinberger, Martin
Feng, Li
Paul, Anita
Smith, Daniel L.
Hontz, Robert D.
Smith, Jeffrey S.
Vujcic, Marija
Singh, Keshav K.
Huberman, Joel A.
Burhans, William C.
Publication Title: 
Cell Cycle (Georgetown, Tex.)

In many organisms, attenuation of growth signaling by caloric restriction or mutational inactivation of growth signaling pathways extends lifespan and protects against cancer and other age-related diseases. The focus of many efforts to understand these effects has been on the induction of oxidative stress defenses that inhibit cellular senescence and cell death. Here we show that in the model organism S.

Author(s): 
Weinberger, Martin
Sampaio-Marques, Belém
Ludovico, Paula
Burhans, William C.
Publication Title: 
BMC complementary and alternative medicine

BACKGROUND: Inhibition of the proteolytic activity of 26S proteasome, the protein-degrading machine, is now considered a novel and promising approach for cancer therapy. Interestingly, proteasome inhibitors have been demonstrated to selectively kill cancer cells and also enhance the sensitivity of tumor cells to chemotherapeutic agents. Recently, polyphenols/flavonoids have been reported to inhibit proteasome activity. Murraya koenigii Spreng, a medicinally important herb of Indian origin, has been used for centuries in the Ayurvedic system of medicine.

Author(s): 
Noolu, Bindu
Ajumeera, Rajanna
Chauhan, Anitha
Nagalla, Balakrishna
Manchala, Raghunath
Ismail, Ayesha
Publication Title: 
BMC complementary and alternative medicine

BACKGROUND: Inhibition of the proteolytic activity of 26S proteasome, the protein-degrading machine, is now considered a novel and promising approach for cancer therapy. Interestingly, proteasome inhibitors have been demonstrated to selectively kill cancer cells and also enhance the sensitivity of tumor cells to chemotherapeutic agents. Recently, polyphenols/flavonoids have been reported to inhibit proteasome activity. Murraya koenigii Spreng, a medicinally important herb of Indian origin, has been used for centuries in the Ayurvedic system of medicine.

Author(s): 
Noolu, Bindu
Ajumeera, Rajanna
Chauhan, Anitha
Nagalla, Balakrishna
Manchala, Raghunath
Ismail, Ayesha
Publication Title: 
The Journal of Biological Chemistry

The mechanisms by which amino acids regulate the cell cycle are not well characterized. In this study, we examined the control of hepatocyte proliferation by amino acids and protein intake. In short-term culture, hepatocytes demonstrated normal entry into S phase and cell cycle protein expression in the absence of essential amino acids. However, deprivation of a set of nonessential amino acids (NEAA) potently inhibited cell cycle progression and selectively down-regulated the expression of proliferation-control proteins.

Author(s): 
Nelsen, Christopher J.
Rickheim, David G.
Tucker, Melissa M.
McKenzie, Travis J.
Hansen, Linda K.
Pestell, Richard G.
Albrecht, Jeffrey H.
Publication Title: 
Molecular cancer research: MCR

Mesothelin (MSLN) is a cell surface glycoprotein that is overexpressed in human pancreatic cancer. Although its value as a tumor marker for diagnosis and prognosis and as a preferred target of immunointervention has been evaluated, there is little information on the growth advantage of MSLN on tumor cells.

Author(s): 
Bharadwaj, Uddalak
Li, Min
Chen, Changyi
Yao, Qizhi
Publication Title: 
Journal of Cell Science

Synthetic lethality is a potential strategy for cancer treatment by specifically promoting the death of cancer cells with particular defects such as the loss of the RB (RB1) tumor suppressor. We previously showed that inactivation of both RB and TSC2 induces synergistic apoptosis during the development of Drosophila melanogaster and in cancer cells. However, the in vivo mechanism of this synthetic-lethal interaction is not clear.

Author(s): 
Gordon, Gabriel M.
Zhang, Tianyi
Zhao, Jiong
Du, Wei
Publication Title: 
Carcinogenesis

Silencing of androgen receptor (AR) signaling is a specific and effective mechanism to cure cancer of the prostate (CaP). In this study, the isolation and characterization of a compound from the aromatic berries of Pimenta dioica (allspice) that silences AR is presented. Potential antitumor activities of an aqueous allspice extract (AAE) and a compound purified from the extract were tested on CaP cells. AAE inhibited tumor cell proliferation and colony formation (50% growth inhibition ∼40-85 µg/ml) but not the viability of quiescent normal fibroblasts or non-tumorigenic prostate cells.

Author(s): 
Shamaladevi, Nagarajarao
Lyn, Dominic A.
Shaaban, Khaled A.
Zhang, Lei
Villate, Susana
Rohr, Jürgen
Lokeshwar, Bal L.

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