Related Experiment Video

Updated: Dec 14, 2025

An In Vitro Protocol for Evaluating MicroRNA Levels, Functions, and Associated Target Genes in Tumor Cells

An In Vitro Protocol for Evaluating MicroRNA Levels, Functions, and Associated Target Genes in Tumor Cells

Published on: May 21, 2019

Downregulation of CDCA3 expression inhibits tumor formation in pancreatic cancer

R C Zou¹, Z T Guo¹, D Wei¹

¹Department of Hepatobiliary Surgery, The Second Affiliated Hospital, Kunming Medical University, Kunming, China.

|July 24, 2020

Abstract:

Downregulation of cell division cycle-associated 3 (CDCA3) markedly inhibited cell growth and induced apoptosis in tumors. However, the effect of CDCA3 in pancreatic cancer (PAC) was rarely investigated. Therefore, this study attempted to clarify the role of CDCA3 in PAC. The mRNA and protein expression of CDCA3 were examined in PAC cell lines and tumor tissues by using real-time quantitative PCR (RT-qPCR), western blotting (WB), and immunohistochemistry (IHC). The effects of CDCA3 downregulation on cell proliferation, apoptosis, and colony information were investigated through MTT assay, Annexin V-APC single staining cell apoptosis detection, and colony formation test. The microarray and ingenuity pathway analysis were employed to explore the potential regulatory relation. The tumor xenograft model was established for determining the effect of CDCA3 downregulation on the growth of PAC in vivo. The results showed that the expression of CDCA3 in tumor tissues was higher than that of normal tissues (p<0.05). In addition, the mRNA expression of CDCA3 was markedly increased in PANC-1 cells and SW 1990 cells when compared with human pancreatic duct epithelial (HPDE) cells (p<0.05). MTT assay showed that the cell proliferation of PANC-1 cells and SW 1990 cells was significantly inhibited after the lentivirus transfection of CDCA3 knockdown (p<0.05). Annexin V-APC apoptosis assays suggested that the apoptotic cell number was markedly increased in the shCDCA3 group compared to that in the shCtrl group in SW 1990 cells and PANC-1 cells (p<0.05). Meanwhile, the activity of caspase-3/7 was obviously elevated in the shCDCA3 group compared to the shCtrl group (p<0.05). The colony formation was notably inhibited in the shCDCA3 group relative to the shCtrl group in SW 1990 cells (p<0.05). Moreover, the tumor growth was evidently suppressed in the shCDCA3 group compared with the shCtrl group in vivo (p<0.05). These findings revealed that CDCA3 plays a crucial role in the progress of PCA by regulating cell apoptosis and proliferation, which may serve as a potential target for PAC treatment.

Insights

Downregulating cell division cycle-associated 3 (CDCA3) inhibits pancreatic cancer growth by increasing apoptosis. This study highlights CDCA3 as a potential therapeutic target for pancreatic cancer (PAC).

Area of Science:

Oncology
Molecular Biology
Cancer Research

Background:

Cell division cycle-associated 3 (CDCA3) is implicated in tumor growth and apoptosis.
The specific role of CDCA3 in pancreatic cancer (PAC) remains largely unexplored.
Understanding CDCA3's function is crucial for developing novel PAC therapies.

Purpose of the Study:

To investigate the role and expression of CDCA3 in pancreatic cancer.
To evaluate the therapeutic potential of targeting CDCA3 in PAC.

Main Methods:

Examined CDCA3 mRNA and protein expression in PAC cell lines and tissues using RT-qPCR, Western Blot, and IHC.
Assessed the impact of CDCA3 knockdown on cell proliferation, apoptosis, and colony formation via MTT, Annexin V assays, and colony formation tests.
Utilized microarray and Ingenuity Pathway Analysis for regulatory pathway exploration and a xenograft model for in vivo validation.

Main Results:

CDCA3 expression was significantly elevated in PAC tissues and cell lines compared to normal tissues and cells.
CDCA3 knockdown markedly inhibited PAC cell proliferation, induced apoptosis (evidenced by increased caspase-3/7 activity), and suppressed colony formation.
In vivo studies demonstrated that CDCA3 downregulation significantly suppressed tumor growth in a xenograft model.

Conclusions:

CDCA3 plays a critical role in the progression of pancreatic cancer by promoting cell proliferation and inhibiting apoptosis.
Downregulation of CDCA3 effectively suppresses pancreatic cancer growth both in vitro and in vivo.
CDCA3 represents a promising therapeutic target for pancreatic cancer treatment.

Read full analysis

More Related Videos

Studying Pancreatic Cancer Stem Cell Characteristics for Developing New Treatment Strategies

Studying Pancreatic Cancer Stem Cell Characteristics for Developing New Treatment Strategies

Published on: June 20, 2015

Author Spotlight: Validating Cancer Therapy Responses with Desmoplastic Spheroid Models

Author Spotlight: Validating Cancer Therapy Responses with Desmoplastic Spheroid Models

Published on: September 27, 2024

Related Concept Videos

Inhibition of Cdk Activity

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...

Abnormal Proliferation

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...

Articles linked to this work by shared authors, journal, and citation graph.

Precision Studies and Searches for CP Asymmetries in the Inclusive Decay Λ_{c}^{+}→ΛX.

Physical review letters·2026

First Energy-Scan Measurement of e^{+}e^{-}→K^{+}K^{-} around the ψ(2S) Resonance.

Physical review letters·2026

First Observation of D^{0(+)}→K[over ¯]ωe^{+}ν_{e} and Determination of the Branching Fraction of K[over ¯]_{1}(1270)→K[over ¯]ω.

Physical review letters·2026

First Experimental Constraint on the Scalar Current in the D^{0(+)}→K[over ¯]ℓ^{+}ν_{ℓ} Transition.

Physical review letters·2026

Measurements of the Absolute Branching Fraction of the Semileptonic Decay Ξ^{-}→Λe^{-}ν[over ¯]_{e} and the Axial Charge of Ξ^{-}.

Physical review letters·2026

Measurement of the Λ electric dipole moment with an entangled baryon-antibaryon system.

Science (New York, N.Y.)·2026

See all related articles