NDLI: Lin-28 reactivation is required for let-7 repression and proliferation in human small cell lung cancer cells

Content Provider	Springer Nature Link
Author	Pan, Lin Gong, Zhaohui Zhong, Zhiwei Dong, Zhuo Liu, Qiong Le, Yanping Guo, Junming
Copyright Year	2011
Abstract	The let-7 family of microRNAs (miRNAs) are known to act as tumor suppressors and down-regulated in lung cancer. Recently, the RNA-binding protein Lin-28 was demonstrated to inhibit biogenesis of let-7 miRNAs by blocking both Drosha- and Dicer-mediated cleavage and accelerating decay of let-7 precursors. We selected NCI-H446 lung small cell lung cancer cell to determine whether it is broadly representative that Lin-28 can promote cell proliferation and affect cell cycle through negatively regulating let-7 biogenesis. Here, we showed that Lin-28 mRNA was up-regulated in NCI-H446 cell with a high c-Myc state. The result of real-time RT-PCR further indicated that pri-let-7a-1/7g and mature let-7g were remarkably down-regulated. The expression of lin-28 was down-regulated while the mature let-7g transcript was up-regulated inversely. The MTT assay indicated that the proliferation of lung cancer cells with lin-28 inhibition was signally impaired. The cells with lin-28 knockdown revealed a higher proportion of cells at G1/G0 phase and less at S phase. The results presented here demonstrate that induction of Lin-28 could mediate repression of let-7 family members, promote cell cycle progression and suppress cell proliferation.
Starting Page	257
Ending Page	263
Page Count	7
File Format	PDF
ISSN	03008177
Journal	Molecular and Cellular Biochemistry
Volume Number	355
Issue Number	1-2
e-ISSN	15734919
Language	English
Publisher	Springer US
Publisher Date	2011-05-07
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Lin-28 Let-7 MicroRNA Small cell lung cancer (SCLC) Cell proliferation Cell cycle Oncology Cardiology Medical Biochemistry Biochemistry
Content Type	Text
Resource Type	Article
Subject	Cell Biology Medicine Clinical Biochemistry Molecular Biology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Selective expression of S100A11 in lung cancer and its role in regulating proliferation of adenocarcinomas cells

High expression of AKR1C1 is associated with proliferation and migration of small-cell lung cancer cells

Etoposide (VP-16) sensitizes p53-deficient human non-small cell lung cancer cells to caspase-7-mediated apoptosis

Combinatorial Action of MicroRNAs let-7 and miR-34 Effectively Synergizes with Erlotinib to Suppress Non-small Cell Lung Cancer Cell Proliferation

Ubiquitin-specific protease 39 is overexpressed in human lung cancer and promotes tumor cell proliferation in vitro

Down-regulation of FBP1 by ZEB1-mediated repression confers to growth and invasion in lung cancer cells

MiR-199a suppresses the hypoxia-induced proliferation of non-small cell lung cancer cells through targeting HIF1α

The let-7 microRNA target gene, Mlin41/Trim71 is required for mouse embryonic survival and neural tube closure

MicroRNA-21 (miR-21) expression promotes growth, metastasis, and chemo- or radioresistance in non-small cell lung cancer cells by targeting PTEN

Lin-28 reactivation is required for let-7 repression and proliferation in human small cell lung cancer cells

Similar Documents

Selective expression of S100A11 in lung cancer and its role in regulating proliferation of adenocarcinomas cells

High expression of AKR1C1 is associated with proliferation and migration of small-cell lung cancer cells

Etoposide (VP-16) sensitizes p53-deficient human non-small cell lung cancer cells to caspase-7-mediated apoptosis

Combinatorial Action of MicroRNAs let-7 and miR-34 Effectively Synergizes with Erlotinib to Suppress Non-small Cell Lung Cancer Cell Proliferation

Ubiquitin-specific protease 39 is overexpressed in human lung cancer and promotes tumor cell proliferation in vitro

Down-regulation of FBP1 by ZEB1-mediated repression confers to growth and invasion in lung cancer cells

MiR-199a suppresses the hypoxia-induced proliferation of non-small cell lung cancer cells through targeting HIF1α

The let-7 microRNA target gene, Mlin41/Trim71 is required for mouse embryonic survival and neural tube closure

MicroRNA-21 (miR-21) expression promotes growth, metastasis, and chemo- or radioresistance in non-small cell lung cancer cells by targeting PTEN

Lin-28 reactivation is required for let-7 repression and proliferation in human small cell lung cancer cells