Subcellular localization of leptin and leptin receptor in breast cancer detected in an electron microscopic study

Al-Shibli, Saad M.; Amjad, Nasser Muhammad; Al-Kubaisi, Muna K.; Mizan, Shaikh

doi:10.1016/j.bbrc.2016.11.165

Cited by 13 publications

(7 citation statements)

References 31 publications

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“…The presence of only high level of circulating LEP cannot be sufficient to produce excessive growth promotion leading to cancer; it must need the receptor. The over-expression of LEPR, as we found in one of our previous studies with breast cancer (Al-Shibli et al, 2017), and by many authors with various cancers (Aloulou et al, 2008; Ishikawa, Kitayama & Nagawa, 2004; Mu et al, 2014; Uchiyama et al, 2011; Uddin et al, 2009b; Jardé et al, 2008; Miyoshi et al, 2006; Uddin et al, 2009a; Hoon Kim et al, 2008) must be significant in the carcinogenic influence of obesity or LEP. However, the claims by various authors about the effect of LEP-LEPR system in colon cancer are confounding, and maybe even contradictory (Hoda et al, 2007; Uchiyama et al, 2011; Stattin et al, 2003; Stattin et al, 2004; Bolukbas et al, 2004; Kumor et al, 2009; Sălăgeanu et al, 2010; Kosova et al, 2013).…”

Section: Discussionsupporting

confidence: 67%

“…As evidence to the above hypothesis, LEP and LEPR have been demonstrated in unusually high concentration in various cancerous tissues by many authors (Koda et al, 2007a). They are found in high concentration in breast carcinoma (O’brien, Welter & Price, 1999; Ishikawa, Kitayama & Nagawa, 2004; Al-Shibli et al, 2017), leukemia (Konopleva et al, 1999), as well as prostate (Saglam et al, 2003), esophagus (Somasundar et al, 2003), gastric (Hong et al, 2006), lung (Ribeiro et al, 2006), adenocarcinomas, etc.…”

Section: Introductionmentioning

confidence: 99%

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Expression of leptin and leptin receptors in colorectal cancer—an immunohistochemical study

Al-Shibli

Harun

Ashour

et al. 2019

PeerJ

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Obesity is demonstrated to be a risk factor in the development of cancers of various organs, such as colon, prostate, pancreas and so on. Leptine (LEP) is the most renowned of the adipokines. As a hormone, it mediates its effect through leptin receptor (LEPR), which is widely expressed in various tissues including colon mucosa. In this study, we have investigated the degree of expression of LEP and LEPR in colorectal cancer (CRC). We collected 44 surgically resected colon cancer tissues along with normal adjacent colon tissue (NACT) from a sample of CRC patients from the Malaysian population and looked for leptin and leptin receptors using immunohistochemistry (IHC). All the samples showed low presence of both LEP and LEPR in NACT, while both LEP and LEPR were present at high intensity in the cancerous tissues with 100% and 97.7% prevalence, respectively. Both were sparsed in the cytoplasm and were concentrated beneath the cell membrane. However, we did not find any significant correlation between their expression and pathological parameters like grade, tumor size, and lymph node involvement. Our study further emphasizes the possible causal role of LEP and LEPR with CRC, and also the prospect of using LEPR as a possible therapeutic target.

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Section: Discussionsupporting

confidence: 67%

Section: Introductionmentioning

confidence: 99%

Expression of leptin and leptin receptors in colorectal cancer—an immunohistochemical study

Al-Shibli

Harun

Ashour

et al. 2019

PeerJ

Self Cite

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“…Presence of only high level of circulating LEP cannot be sufficient to produce excessive growth promotion leading to cancer, it must need the receptor. The over-expression of LEPR, as we found in one of our previous studies with breast cancer (68), and by many authors with various cancers (46,67,(85)(86)(87)90,(93)(94)(95) must be significant in the carcinogenic influence of obesity or LEP. However, the claims by various authors about the effect of LEP-LEPR system in colon cancer are confounding, and maybe even contradictory (82,86,(96)(97)(98)(99)(100)(101).…”

Section: Discussionsupporting

confidence: 64%

Peer Review #1 of "Expression of leptin and leptin receptors in colorectal cancer—an immunohistochemical study (v0.1)"

Basu¹

2019

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Obesity is demonstrated to be a risk factor in the development of cancers of various organs, such as colon, prostate, pancreas and so on. Leptine (LEP) is the most renowned of the adipokines. As a hormone, it mediates its effect through leptin receptor (LEPR), which is widely expressed in various tissues including colon mucosa. In this study, we have investigated the degree of expression of LEP and LEPR in colorectal cancer (CRC). We collected 44 surgically resected colon cancer tissues along with normal adjacent colon tissue (NACT) from a sample of CRC patients from Malaysian population and looked for leptin and leptin receptor using immunohistochemistry (IHC). All the samples showed low presence of both LEP and LEPR in NACT. While both LEP and LEPR were present at high intensity in the cancerous tissues with 100% and 97.7% prevalence respectively. Both were sparsed in the cytoplasm and were concentrated beneath the cell membrane. However, we did not find any significant correlation between their expression and pathological parameters like grade, tumor size, and lymph node involvement. Our study further emphasizes the possible causal role of LEP and LEPR with CRC, and also the prospect of using LEPR as a possible therapeutic target.

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“…The browning response induced with low temperature was associated with leptin translocation to the nucleus of UCP1 positive adipocytes, indicating a possible role for leptin in the browning process. The nuclear presence of leptin receptors has also been observed in a different cellular context 45 , suggesting a possible new regulatory role for leptin, a hypothesis consistent with its reported stimulatory effect on fatty acid oxidation 46 .…”

Section: Discussionmentioning

confidence: 52%

Low temperature exposure induces browning of bone marrow stem cell derived adipocytes in vitro

Veličković

Leija

Bloor

et al. 2018

Sci Rep

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Brown and beige adipocytes are characterised as expressing the unique mitochondrial uncoupling protein (UCP)1 for which the primary stimulus in vivo is cold exposure. The extent to which cold-induced UCP1 activation can also be achieved in vitro, and therefore perform a comparable cellular function, is unknown. We report an in vitro model to induce adipocyte browning using bone marrow (BM) derived mesenchymal stem cells (MSC), which relies on differentiation at 32 °C instead of 37 °C. The low temperature promoted browning in adipogenic cultures, with increased adipocyte differentiation and upregulation of adipogenic and thermogenic factors, especially UCP1. Cells exhibited enhanced uncoupled respiration and metabolic adaptation. Cold-exposed differentiated cells showed a marked translocation of leptin to adipocyte nuclei, suggesting a previously unknown role for leptin in the browning process. These results indicate that BM-MSC can be driven to forming beige-like adipocytes in vitro by exposure to a reduced temperature. This in vitro model will provide a powerful tool to elucidate the precise role of leptin and related hormones in hitherto functions in the browning process.

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Subcellular localization of leptin and leptin receptor in breast cancer detected in an electron microscopic study

Cited by 13 publications

References 31 publications

Expression of leptin and leptin receptors in colorectal cancer—an immunohistochemical study

Expression of leptin and leptin receptors in colorectal cancer—an immunohistochemical study

Peer Review #1 of "Expression of leptin and leptin receptors in colorectal cancer—an immunohistochemical study (v0.1)"

Low temperature exposure induces browning of bone marrow stem cell derived adipocytes in vitro

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