Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Targeted Cancer Therapies

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...

Treatment Resistant Cancers

Treatment Resistant Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...

Pharmacogenetics of Drug Transporters: P-Glycoprotein and Solute Carrier Transporters

Pharmacogenetics of Drug Transporters: P-Glycoprotein and Solute Carrier Transporters

The pharmacogenetics of drug transporters is increasingly recognized as a critical factor influencing interindividual variability in drug absorption, distribution, and elimination. These membrane-bound proteins regulate drugs' movement across cellular barriers by actively pumping them out (efflux) or facilitating their uptake (influx). Among the major transporter families, ATP-binding cassette (ABC) and solute carrier (SLC) transporters play particularly prominent roles. Genetic polymorphisms...

You might also read

Related Articles

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

Sort by

Same author

Radiocontrast agent and intraductal pressure promote the progression of post-ERCP pancreatitis by regulating inflammatory response, cellular apoptosis, and tight junction integrity.

Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]·2021

Same author

Occurrence and fate of polycyclic aromatic hydrocarbons from electronic waste dismantling activities: A critical review from environmental pollution to human health.

Journal of hazardous materials·2021

Same author

ATG16L2 overexpression is associated with a good prognosis in colorectal cancer.

Journal of gastrointestinal oncology·2021

Same author

A Novel Pyroptosis-Related Gene Signature for Prognostic Prediction of Head and Neck Squamous Cell Carcinoma.

International journal of general medicine·2021

Same author

Application of dermal regenerative template in reconstructing skin defects after plantar malignant melanoma excision.

Journal of B.U.ON. : official journal of the Balkan Union of Oncology·2021

Same author

Multi-alleles predict primary non-response to infliximab therapy in Crohn's disease.

Gastroenterology report·2021

Search research articles

Related Experiment Video

Updated: Jun 12, 2026

Site-Specific Lysine Lactylation via Genetic Code Expansion in E. coli and Mammalian Cells

Site-Specific Lysine Lactylation via Genetic Code Expansion in E. coli and Mammalian Cells

Published on: February 24, 2026

SLC16A9-Mediated Carnitine Uptake Enhances Radiotherapy Resistance in Colorectal Cancer via Lipid Metabolic

Meng Wang¹, Jian Tang², Xing Wen¹

¹Center of Gastrointestinal and Minimally Invasive Surgery, Department of General Surgery, The Third People's Hospital of Chengdu, Affiliated Hospital of Southwest Jiaotong University & The Second Affiliated Hospital of Chengdu, Chongqing Medical University, Chengdu, China.

Comprehensive Physiology

|June 10, 2026

Summary

The transporter SLC16A9 promotes colorectal cancer radioresistance by enhancing fatty acid oxidation (FAO) and carnitine uptake. Targeting SLC16A9 or FAO may improve radiotherapy efficacy.

Keywords:

SLC16A9 carnitine colorectal cancer fatty acid oxidation lipid metabolic reprogramming radioresistance

Related Experiment Videos

Last Updated: Jun 12, 2026

Site-Specific Lysine Lactylation via Genetic Code Expansion in E. coli and Mammalian Cells

Site-Specific Lysine Lactylation via Genetic Code Expansion in E. coli and Mammalian Cells

Published on: February 24, 2026

Area of Science:

Oncology
Molecular Biology
Metabolism

Background:

Radiation resistance is a major challenge in colorectal cancer (CRC) radiotherapy.
Fatty acid oxidation (FAO) is implicated in radioresistance, but regulatory mechanisms are unclear.

Purpose of the Study:

To investigate the role of solute carrier family 16 member 9 (SLC16A9) in CRC radioresistance.
To explore the link between SLC16A9, carnitine metabolism, and FAO.

Main Methods:

Analysis of transcriptomic databases and clinical CRC samples.
In vitro assays (CCK-8, colony formation, comet, apoptosis) to assess radiosensitivity.
In vivo xenograft models to evaluate tumor response to radiotherapy.

Main Results:

SLC16A9 was upregulated in radioresistant CRC cells and tissues.
SLC16A9 enhanced carnitine uptake and FAO activity, reducing DNA damage and increasing survival.
SLC16A9 inhibition improved radiosensitivity in vitro and in vivo.

Conclusions:

SLC16A9 drives CRC radioresistance by promoting carnitine uptake and FAO.
SLC16A9 and FAO are potential therapeutic targets to overcome radioresistance in CRC.