Abolition of Cyclin-Dependent Kinase Inhibitor p16Ink4a and p21Cip1/Waf1 Functions Permits Ras-Induced Anchorage-Independent Growth in Telomerase-Immortalized Human Fibroblasts

Wei, Wenyi; Jobling, Wendy A.; Chen, Wen; Hahn, William C.; Sedivy, John M.

doi:10.1128/mcb.23.8.2859-2870.2003

Cited by 69 publications

(73 citation statements)

References 80 publications

(112 reference statements)

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“…They are associated with progression of variable tumors; miR-106a and miR-106b in gastric adenocarcinoma [29], miR-17-5p and miR-372 in squamous cell carcinoma [30], miR-372 and miR-373 in testicular germ cell tumors [10], and miR-373 with miR-520c in the metastatic tumors [31]. Moreover, inactivation of p21 and p16 INK4a facilitates immortalization and anchorage independent growth of mouse fibroblasts [11]. The data well support our present report, because foreskin HDF rarely expresses p16 INK4a .…”

Section: Discussionmentioning

confidence: 99%

“…p21 is involved in the Ras G12V -induced senescence in different human cells; inhibition of p21 expression results in Ras G12V -resistant growth in BJ foreskin fibroblasts [10] and LF1 human lung fibroblasts [11]. Treatment of various human cells with low dose doxorubicin (200 ng/ml) also induces growth arrest with high expressions of p53 and p21 [12].…”

Section: Introductionmentioning

confidence: 99%

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Loss of p21Sdi1 expression in senescent cells after DNA damage accompanied with increase of miR-93 expression and reduced p53 interaction with p21Sdi1 gene promoter

Choi

Lim

2011

Biochemical and Biophysical Research Communications

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Loss of p21Sdi1 expression in senescent cells after DNA damage accompanied with increase of miR-93 expression and reduced p53 interaction with p21Sdi1 gene promoter

Choi

Lim

2011

Biochemical and Biophysical Research Communications

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“…These experiments suggest that loss of p53 and p16 INK4A function is not equivalent to LT expression in transformation (Wei et al 2003). Differences between the cell lines used and/or the methods of p53 and RB pathway perturbation may, in part, explain these divergent conclusions.…”

Section: Sv40 Lt Antigen: Inhibiting the Rb/p16 Ink4a And P53/p14 Arfmentioning

confidence: 93%

“…In contrast, Wei et al (2003) addressed this issue by expressing a cyclin D1-CDK4 R24C fusion protein in LF1 lung fibroblasts. Expression of the cyclin D1-CDK4 R24C fusion protein renders the cells insensitive to p16 INK4A , yet fails to cooperate with the co-expression of hTERT, ST, and RAS to transform a p53 null LF1 line.…”

Section: Sv40 Lt Antigen: Inhibiting the Rb/p16 Ink4a And P53/p14 Arfmentioning

confidence: 99%

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Immortalized cells as experimental models to study cancer

Boehm

Hahn

2004

Cytotechnology

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The development of cancer is a multi-step process in which normal cells sustain a series of genetic alterations that together program the malignant phenotype. Much of our knowledge of cancer biology results from the detailed study of specimens and cell lines derived from patient tumors. While these approaches continue to yield critical information regarding the identity, number, and types of alterations found in human tumors, further progress in understanding the molecular basis of malignant transformation depends upon the generation and use of increasingly sophisticated experimental models of cancer. Over the past several years, the recognition that telomeres and telomerase play essential roles in regulating cell lifespan now permits the development of new models of human cancer. Here we review recent progress in the use of immortalized human cells as a foundation for understanding the molecular basis of cancer.Abbreviations: ALT -alternative lengthening of telomeres; HEK -human embryonic kidney; HMEChuman mammary epithelial cell; HPV -human papillomavirus; hTERT -human telomerase reverse transcriptase; LT -SV40 Large T antigen; PD -population doubling; PP2A -protein phosphatase 2A; RalGEF -Ral guanine nucleotide exchange factor; RAS -activated H-Ras allele; shRNA -short hairpin RNA; ST -SV40 small t antigen; TRF -telomere restriction fragment.

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Ribosomal Proteins Control Tumor Suppressor Pathways in Response to Nucleolar Stress

2019

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Ribosome biogenesis includes the making and processing of ribosomal RNAs, the biosynthesis of ribosomal proteins from their mRNAs in the cytosol and their transport to the nucleolus to assemble pre‐ribosomal particles. Several stresses including cellular senescence reduce nucleolar rRNA synthesis and maturation increasing the availability of ribosome‐free ribosomal proteins. Several ribosomal proteins can activate the p53 tumor suppressor pathway but cells without p53 can still arrest their proliferation in response to an imbalance between ribosomal proteins and mature rRNA production. Recent results on senescence‐associated ribogenesis defects (SARD) show that the ribosomal protein S14 (RPS14 or uS11) can act as a CDK4/6 inhibitor linking ribosome biogenesis defects to the main engine of cell cycle progression. This work offers new insights into the regulation of the cell cycle and suggests novel avenues to design anticancer drugs.

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Abolition of Cyclin-Dependent Kinase Inhibitor p16^Ink4a and p21^Cip1/Waf1 Functions Permits Ras-Induced Anchorage-Independent Growth in Telomerase-Immortalized Human Fibroblasts

Cited by 69 publications

References 80 publications

Loss of p21Sdi1 expression in senescent cells after DNA damage accompanied with increase of miR-93 expression and reduced p53 interaction with p21Sdi1 gene promoter

Loss of p21Sdi1 expression in senescent cells after DNA damage accompanied with increase of miR-93 expression and reduced p53 interaction with p21Sdi1 gene promoter

Immortalized cells as experimental models to study cancer

Ribosomal Proteins Control Tumor Suppressor Pathways in Response to Nucleolar Stress

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